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Sample records for tau decay tau

  1. Review of tau lepton decays

    SciTech Connect

    Stoker, D.P.

    1991-07-01

    Measurements of the {tau} decay modes are reviewed and compared with the predictions of the Standard Model. While the agreement is generally good, the status of the 1-prong puzzle'' remains controversial and a discrepancy between the measured leptonic branching fractions and the {tau} lifetime persists. Prospects for precision measurements at a Tau-Charm Factory are also reviewed. 20 refs., 2 tabs.

  2. Tau decays: A theoretical perspective

    SciTech Connect

    Marciano, W.J.

    1992-11-01

    Theoretical predictions for various tau decay rates are reviewed. Effects of electroweak radiative corrections are described. Implications for precision tests of the standard model and ``new physics`` searches are discussed. A perspective on the tau decay puzzle and 1-prong problem is given.

  3. Tau decays: A theoretical perspective

    SciTech Connect

    Marciano, W.J.

    1992-11-01

    Theoretical predictions for various tau decay rates are reviewed. Effects of electroweak radiative corrections are described. Implications for precision tests of the standard model and new physics'' searches are discussed. A perspective on the tau decay puzzle and 1-prong problem is given.

  4. tau. r arrow. omega. pi. nu. sub. tau. decay

    SciTech Connect

    Fajfer, S.; Suruliz, K. ); Oakes, R.J. )

    1992-08-01

    The decay width for {tau}{r arrow}{omega}{pi}{nu}{sub {tau}} is calculated using a general low-energy effective Lagrangian for pseudoscalar and vector mesons with U(3){times}U(3) chiral symmetry. The relevant couplings are determined empirically from vector-meson decays. A comparison with results coming from the vector-meson-dominance model is given.

  5. The tau decay mode problem

    SciTech Connect

    Perl, M.L.

    1988-05-01

    The problem of understanding the branching fractions of the 1-charged particle decay modes of the /tau/ lepton is reviewed. The emphasis is on a recent study by K.G. Hayes and M.L. Perl of the statistical validity of the branching fraction measurements. Unconventional explanations of the problem, none of them satisfactory, are also discussed. 25 refs., 4 tabs.

  6. Tau Decays at BaBar

    SciTech Connect

    Hast, Carsten; ,

    2009-01-22

    Recent results of tau lepton decay studies based on luminosities between 350 fb{sup -1} and 469 fb{sup -1} collected with the BABAR detector at the PEP-II e{sup +}e{sup -} collider at the SLAC National Accelerator Laboratory are presented. The analyses reported here are Charged Current Lepton Universality and measurements of |V{sub us}| using {tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}, {mu}{sup -}{bar {nu}}{sub {mu}}{nu}{sub {tau}}, {pi}{sup -} {nu}{sub {tau}}, and K{sup -}{nu}{sub {tau}} decays, as well as searches for Second Class Currents in {tau}{sup -} {yields} {omega}{pi}{sup -}{nu}{sub {tau}} decays, studies of Lepton Flavor Violations, and a tau mass measurement and CPT-Test. If not explicitly mentioned, charge conjugate decay modes are also implied. decays, as well as searches for Second Class Currents in {tau}{sup -} {yields} {omega}{pi}{sup -}{nu}{sub {tau}} decays, studies of Lepton Flavor Violations, and a tau mass measurement and CPT-Test. If not explicitly mentioned, charge conjugate decay modes are also implied.

  7. B to tau Leptonic and Semileptonic Decays

    SciTech Connect

    Barrett, M.; /Brunel U.

    2011-11-17

    Decays of B mesons to states involving {tau} leptons can be used as a tool to search for the effects of new physics, such as those involving a charged Higgs boson. The experimental status of the decays B {yields} {tau}{nu} and B {yields} D{sup (*)}{tau}{nu} is discussed, together with limits on new physics effects from current results. Leptonic and semileptonic decays of B mesons into states involving {tau} leptons remain experimentally challenging, but can prove a useful tool for constraining Standard Model parameters, and also offer to constrain the effects of any new physics that may exist including the presence of a charged Higgs boson.

  8. Crystal Ball results on tau decays

    SciTech Connect

    Lowe, S.T.

    1987-10-01

    This report reviews measurements and upper limit determinations for a number of exclusive 1-prong tau decay modes using the Crystal Ball detector. These results are important input to the apparent discrepancy between the topological and sum-of-exclusive branching fractions in 1-prong tau decays.

  9. Precision Measurements of Tau Lepton Decays

    SciTech Connect

    Nugent, Ian M.; /Victoria U.

    2010-03-16

    Using data collected with the BABAR detector at the SLAC PEP-II electron-positron storage ring operating at a center-of-mass energy near 10.58 GeV, the branching fractions {Beta}({tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{nu}{sub {tau}}) = (8.83 {+-} 0.01 {+-} 0.13)%, {Beta}({tau}{sup -} {yields} K{sup -}{pi}{sup -}{pi}{sup +}{nu}{sub {tau}}) = (0.273 {+-} 0.002 {+-} 0.009)%, {Beta}({tau}{sup -} {yields} K{sup -}{pi}{sup -}K{sup +}{nu}{sub {tau}}) = (0.1346 {+-} 0.0010 {+-} 0.0036)%, and {Beta}({tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu}{sub {tau}}) = (1.58 {+-} 0.13 {+-} 0.12) x 10{sup -5} are measured where the uncertainties are statistical and systematic, respectively. The invariant mass distribution for the {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{nu}{sub {tau}} {yields} K{sup -}{pi}{sup -}{pi}{sup +}{nu}{sub {tau}}, {tau}{sup -} {yields} K{sup -}{pi}{sup -}K{sup +}{nu}{sub {tau}} and {tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu}{sub {tau}} decays are unfolded to correct for detector effects. A measurement of {Beta}({tau}{sup -} {yields} {phi}{pi}{sup -}{nu}{sub {tau}}) = (3.42 {+-} 0.55 {+-} 0.25) x 10{sup -5}, a measurement of {Beta}({tau}{sup -} {yields} {phi}K{sup -}{nu}{sub {tau}}) = (3.39 {+-} 0.20 {+-} 0.28) x 10{sup -5} and an upper limit on {Beta}({tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu}{sub {tau}}[ex.{phi}]) {le} 2.5 x 10{sup -6} {at} 905 CL are determined from a binned maximum likelihood fit of the {tau}{sup -} {yields} K{sup -}{pi}{sup -}K{sup +}{nu}{sub {tau}} and {tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu}{sub {tau}} K{sup +}K{sup -} invariant mass distributions. The branching ratio {Beta}({tau}{sup -} {yields} K{sup -}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} {pi}{sup -}{nu}{sub {tau}}) is measured to be (6.531 {+-} 0.056 {+-} 0.093) x 10{sup -2} from which |V{sub us}| is determined to be 0.2255 {+-} 0.0023. The branching ratio {Beta}/({tau}{sup -} {yields} {mu}{nu}{sub {tau}}{bar {nu}}{sub {mu}})/{Beta}({tau}{sup -} {yields} e{sup -} {nu}{sub {tau}}{bar {nu}}{sub e}) = (9.796 {+-} 0.016 {+-} 0.035) x 10{sup -1} is measured enabling a precision test of the Standard Model assumption of charged current lepton universality, g{sub {mu}}/g{sub e} = 1.0036 {+-} 0.0020. The branching ratios {Beta}({tau}{sup -} {yields} K{sup -}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -}{nu}{sub {tau}}{bar {nu}}{sub e}) = (3.882 {+-} 0.032 {+-} 0.057) x 10{sup -2}, and {Beta}({tau}{sup -} {yields} {pi}{sup -}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{nu}{sub {tau}}{bar {nu}}{sub e}) = (5.9545 {+-} 0.014 {+-} 0.061) x 10{sup -1} are measured which provide additional tests of charged current lepton universality, (g{sub {tau}}/g{sub {mu}}){sub {pi}} = 0.9856 {+-} 0.0057 and (g{sub {tau}}/g{sub {mu}}){sub K} = 0.9827 {+-} 0.0086 which can be combined to give (g{sub {tau}}/g{sub {mu}}){sub {pi}/K} = 0.9850 {+-} 0.0054. Any deviation of these measurements from the expected Standard Model values would be an indication of new physics.

  10. Tensor mesons produced in tau lepton decays

    SciTech Connect

    Lopez Castro, G.; Munoz, J. H.

    2011-05-01

    Light tensor mesons (T=a{sub 2}, f{sub 2} and K{sub 2}*) can be produced in decays of {tau} leptons. In this paper we compute the branching ratios of {tau}{yields}T{pi}{nu} decays by assuming the dominance of intermediate virtual states to model the form factors involved in the relevant hadronic matrix elements. The exclusive f{sub 2}(1270){pi}{sup -} decay mode turns out to have the largest branching ratio, of O(10{sup -4}). Our results indicate that the contribution of tensor meson intermediate states to the three-pseudoscalar channels of {tau} decays are rather small.

  11. Evidence for B+ --> tau+ nu_tau Decays using Hadronic B Tags

    SciTech Connect

    del Amo Sanchez, P.; Lees, J.P.; Poireau, V.; Prencipe, E.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Milanes, D.A.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; Koch, H.; Schroeder, T.; /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Indian Inst. Tech., Guwahati /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /INFN, Naples /Naples U. /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Southern Methodist U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2011-08-11

    We present a search for the decay B{sup +} --> {tau}{sup +} {nu}{sub {tau}} using 467.8 x 10{sup 6} B{anti B} pairs collected at the {Upsilon}(4S) resonance with the BABAR detector at the SLAC PEP-II B-Factory. We select a sample of events with on completely reconstructed B{sup -} in an hadronic decay mode (B{sup -} --> D{sup (*)0}X{sup -} and B{sup -} --> J/{psi} X{sup -}). We examine the rest of the event to search for a B{sup +} --> {tau}{sup +} {nu}{sub {tau}} decay. We identify the {tau}{sup +} lepton in the following modes: {tau}{sup +} --> e{sup +} {nu}{sub e}{anti {nu}}{sub {tau}}, {tau}{sup +} --> {mu}{sup +} {nu}{sub {mu}}{anti {nu}}{sub {tau}}, {tau}{sup +} --> {pi}{sup +}{anti {nu}}{sub {tau}} and {tau}{sup +} --> {rho}{anti {nu}}{sub {tau}}. We find an excess of events with respect to expected background, which excludes the null signal hypothesis at the level of 3.3 {sigma} and can be converted to a branching fraction central value of B(B{sup +} --> {tau}{sup +} {nu}{sub {tau}})= (1.80{sup + 0.57}{sub - 0.54}(stat.) {+-} 0.26 (syst.)) x 10{sup -4}.

  12. Reconstruction and selection of Z{yields}{tau}{tau}{yields}{mu}+{tau}-jet+{nu}'s decays at the CMS experiment

    SciTech Connect

    Lusito, Letizia

    2010-12-22

    At the LHC, tau leptons are expected in final states of many important physics processes including Supersymmetry and the production of Higgs boson(s) and other exotic particles. An efficient and accurate {tau} reconstruction and identification are therefore an important part of the CMS physics programme. Z{sup 0}{yields}{tau}{sup +}{tau}{sup -} decays are often considered the ''standard candle'' of tau reconstruction as they validate tau lepton identification and provide a test bench for Higgs searches (for which they constitute the main irreducible background). We describe techniques for selecting and reconstructing the Z{sup 0}{yields}{tau}{sup {+-}}{tau}{sup {-+}}{yields}{mu}{sup {+-}}{nu}{sub {mu}}{bar {nu}}{sub {tau}}({bar {nu}}{sub {mu}}{nu}{sub {tau}})+{tau}-jet{sup {-+}}{nu}{sub {tau}}({bar {nu}}{sub {tau}}) events that were developed for the measurement of the Z production cross-section by the CMS experiment using 200 pb{sup -1} of the LHC collision data at the center-of-mass energy {radical}(s) 10 TeV. We validate these techniques using simulated events and present a data-driven method for estimating background contributions to this measurement.

  13. Addendum to the test of CP violation in Tau decay

    SciTech Connect

    Tsai, Yung Su

    1995-08-01

    We discuss the test of CP and CPT violation in Tau decay without using the polarized electron beam by comparing partial fractions of tau(-) and tau(+) decay into channels with strong final state interactions. For example, gamma(tau(-) right arrow pi(-) + pi(0) + nu) not equal gamma(tau(+) right arrow pi(+) + pi(0) + nu) signifies violation of CP. The optimum energy to investigate CP violation in tau decay is discussed. We conclude that this energy is a few MeV below psi(2s) in order to avoid the charm contribution and over abundance of hadrons at the psi(2s) peak.

  14. A Search for the Rare Decay B0 to tau+tau- atBaBar

    SciTech Connect

    Aubert, B.; Barate, R.; Boutigny, D.; Couderc, F.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Tisserand, V.; Zghiche, A.; Grauges, E.; Palano, A.; Pappagallo, M.; Pompili, A.; Chen, J.C.; Qi, N.D.; Rong, G.; Wang, P.; Zhu, Y.S.; Eigen, G.; Ofte, I.; Stugu, B. /Bergen U. /LBL, Berkeley /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /Bristol U. /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, AUTHOR = Roethel, W. /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /DSM, DAPNIA, Saclay /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /Ferrara U. /INFN, Ferrara /Frascati /Genoa U. /INFN, Genoa /Harvard U. /Heidelberg U. /Valencia U., IFIC /Imperial Coll., London /Iowa U. /Iowa State U. /INFN, Perugia /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT, LNS /McGill U. /Milan U. /INFN, Milan /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /NIKHEF, Amsterdam /Naples U. /INFN, Naples /Notre Dame U. /Ohio State U. /Oregon U. /Padua U. /INFN, Padua /Paris U., VI-VII /Pennsylvania U. /Pisa U. /Pisa, Scuola Normale Superiore /INFN, Pisa /Prairie View A-M /Princeton U. /Rome U. /INFN, Rome /Rostock U. /Rutherford /South Carolina U. /SLAC /Stanford U., Phys. Dept. /SUNY, Albany /Tennessee U. /Texas U. /Texas U., Dallas /Turin U. /INFN, Turin /Trieste U. /INFN, Trieste /Vanderbilt U. /Victoria U. /Warwick U. /Wisconsin U., Madison /Yale U. /Karlsruhe U., EKP

    2005-11-09

    We present the results of a search for the decay B{sup 0} {yields} {tau}{sup +}{tau}{sup -} in a data sample of (232 {+-} 3) x 10{sup 6} {Upsilon}(4S) {yields} B{bar B} decays using the BABAR detector. Certain extensions of the Standard Model predict measurable levels of this otherwise rare decay. We reconstruct fully one neutral B meson and seek evidence for the signal decay in the rest of the event. We find no evidence for signal events and obtain {Beta}(B{sup 0} {yields} {tau}{sup +}{tau}{sup -}) < 3.2 x 10{sup -3} at the 90% confidence level.

  15. Search for the rare decay B0-->tau+tau- at BABAR.

    PubMed

    Aubert, B; Barate, R; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Pappagallo, M; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Chevalier, N; Cottingham, W N; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, A E; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Mommsen, R K; Roethel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Weinstein, A J R; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; del Re, D; Hadavand, H K; Hill, E J; MacFarlane, D B; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nauenberg, U; Olivas, A; Rankin, P; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Harton, J L; Soffer, A; Toki, W H; Wilson, R J; Zeng, Q; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Giraud, P-F; Graziani, G; Hamel de Monchenault, G; Kozanecki, W; Legendre, M; London, G W; Mayer, B; Vasseur, G; Yeche, Ch; Zito, M; Altenburg, D; Feltresi, E; Hauke, A; Spaan, B; Brandt, T; Brose, J; Dickopp, M; Klose, V; Lacker, H M; Nogowski, R; Otto, S; Petzold, A; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Bernard, D; Bonneaud, G R; Grenier, P; Schrenk, S; Thiebaux, Ch; Vasileiadis, G; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Xie, Y; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Piemontese, L; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Patteri, P; Peruzzi, I M; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Won, E; Wu, J; Dubitzky, R S; Langenegger, U; Marks, J; Schenk, S; Uwer, U; Martinez-Vidal, F; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Morton, G W; Nash, J A; Nikolich, M B; Taylor, G P; Vazquez, W P; Charles, M J; Mader, W F; Mallik, U; Mohapatra, A K; Cochran, J; Crawley, H B; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Yi, J; Biasini, M; Covarelli, R; Pacetti, S; Pioppi, M; Arnaud, N; Davier, M; Giroux, X; Grosdidier, G; Höcker, A; Le Diberder, F; Lepeltier, V; Lutz, A M; Oyanguren, A; Petersen, T C; Pierini, M; Plaszczynski, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Chavez, C A; Forster, Ian J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Parry, R J; Payne, D J; Schofield, K C; Touramanis, C; Cormack, C M; Di Lodovico, F; Menges, W; Sacco, R; Brown, C L; Cowan, G; Flaecher, H U; Green, M G; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Edgar, C L; Hodgkinson, M C; Kelly, M P; Lafferty, G D; Naisbit, M T; Williams, J C; Chen, C; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Kofler, R; Koptchev, V B; Li, X; Moore, T B; Saremi, S; Staengle, H; Willocq, S; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Cote, D; Taras, P; Viaud, B; Nicholson, H; Baak, M; Bulten, H; Raven, G; Snoek, H L; Wilden, L; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Jessop, C P; LoSecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonyan, R; Wong, Q K; Brau, J; Frey, R; Igonkina, O; Lu, M; Potter, C T; Sinev, N B; Strom, D; Strube, J; Torrence, E; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; de la Vaissiere, C; Del Buono, L; Hamon, O; John, M J J; Leruste, Ph; Malcles, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Morganit, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Safai Tehrani, F; Voena, C; Schröder, H; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Gopal, G P; Olaiya, E O; Wilson, F F; Purohit, M V; Weidemann, A W; Wilson, J R; Yumiceva, F X; Abe, T; Allen, M T; Aston, D; Bartoldus, R; Berger, N; Boyarski, A M; Buchmueller, O L; Claus, R; Coleman, J P; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W; Fan, S; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Luth, V; Lynch, H L; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; van Bakel, N; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Ahmed, M; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bona, M; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Panvini, R S; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Graham, M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihalyi, A; Pan, Y; Prepost, R; Tan, P; von Wimmersperg-Toeller, J H; Wu, S L; Yu, Z; Neal, H; Schott, G

    2006-06-23

    We present the results of a search for the decay B0-->tau+tau- in a data sample of (232+/-3)x10(6) Upsilon(4S)-->BB decays using the BABAR detector. Certain extensions of the standard model predict measurable levels of this otherwise rare decay. We reconstruct fully one neutral B meson and seek evidence for the signal decay in the rest of the event. We find no evidence for signal events and obtain Beta(B0->tau+tau-)<4.1x10(-3) at the 90% confidence level. PMID:16907230

  16. Observation of Upsilon(3S)-->tau+tau- and tests of lepton universality in Upsilon decays.

    PubMed

    Besson, D; Pedlar, T K; Cronin-Hennessy, D; Gao, K Y; Gong, D T; Hietala, J; Kubota, Y; Klein, T; Lang, B W; Poling, R; Scott, A W; Smith, A; Zweber, P; Dobbs, S; Metreveli, Z; Seth, K K; Tomaradze, A; Ernst, J; Severini, H; Dytman, S A; Love, W; Savinov, V; Aquines, O; Li, Z; Lopez, A; Mehrabyan, S; Mendez, H; Ramirez, J; Huang, G S; Miller, D H; Pavlunin, V; Sanghi, B; Shipsey, I P J; Xin, B; Adams, G S; Anderson, M; Cummings, J P; Danko, I; Napolitano, J; He, Q; Insler, J; Muramatsu, H; Park, C S; Thorndike, E H; Yang, F; Coan, T E; Gao, Y S; Liu, F; Artuso, M; Blusk, S; Butt, J; Horwitz, N; Li, J; Menaa, N; Mountain, R; Nisar, S; Randrianarivony, K; Redjimi, R; Sia, R; Skwarnicki, T; Stone, S; Wang, J C; Zhang, K; Csorna, S E; Bonvicini, G; Cinabro, D; Dubrovin, M; Lincoln, A; Asner, D M; Edwards, K W; Briere, R A; Brock, I; Chen, J; Ferguson, T; Tatishvili, G; Vogel, H; Watkins, M E; Rosner, J L; Adam, N E; Alexander, J P; Berkelman, K; Cassel, D G; Duboscq, J E; Ecklund, K M; Ehrlich, R; Fields, L; Galik, R S; Gibbons, L; Gray, R; Gray, S W; Hartill, D L; Heltsley, B K; Hertz, D; Jones, C D; Kandaswamy, J; Kreinick, D L; Kuznetsov, V E; Mahlke-Krger, H; Meyer, T O; Onyisi, P U E; Patterson, J R; Peterson, D; Pivarski, J; Riley, D; Ryd, A; Sadoff, A J; Schwarthoff, H; Shi, X; Stroiney, S; Sun, W M; Wilksen, T; Weinberger, M; Athar, S B; Patel, R; Potlia, V; Yelton, J; Rubin, P; Cawlfield, C; Eisenstein, B I; Karliner, I; Kim, D; Lowrey, N; Naik, P; Sedlack, C; Selen, M; White, E J; Wiss, J; Shepherd, M R

    2007-02-01

    Using data collected with the CLEO III detector at the CESR e+e- collider, we report on a first observation of the decay Upsilon(3S)-->tau+tau-, and precisely measure the ratio of branching fractions of Upsilon(nS), n=1, 2, 3, to tau+tau- and mu+mu- final states, finding agreement with expectations from lepton universality. We derive absolute branching fractions for these decays, and also set a limit on the influence of a low mass CP-odd Higgs boson in the decay of the Upsilon(1S). PMID:17358847

  17. Unraveling duality violations in hadronic tau decays

    SciTech Connect

    Cata, Oscar; Cata, Oscar; Golterman, Maarten; Peris, Santiago

    2008-03-03

    There are some indications from recent determinations of the strong coupling constant alpha_s and the gluon condensate that the Operator Product Expansion may not be accurate enough to describe non-perturbative effects in hadronic tau decays. This breakdown of the Operator Product Expansion is usually referred to as being due to"Duality Violations." With the help of a physically motivated model, we investigate these duality violations. Based on this model, we argue how they may introduce a non-negligible systematic error in the current analysis, which employs finite-energy sum rules with pinched weights. In particular, this systematic effect might affect the precision determination of alpha_s from tau decays. With a view to a possible future application to real data, we present an alternative method for determining the OPE coefficients that might help estimating, and possibly even reducing, this systematic error.

  18. Measurement of the Semileptonic Decays B->D tau nu and B->D* tau nu

    SciTech Connect

    Aubert, : B.

    2009-02-23

    The authors present measurements of the semileptonic decays B{sup -} {yields} D{sup 0} {tau}{sup -} {bar {nu}}{sub {tau}}, B{sup -} {yields} D*{sup 0} {tau}{sup -}{bar {nu}}{sub {tau}}, {bar B}{sup 0} {yields} D{sup +} {tau}{sup -} {bar {nu}}{sub {tau}}, and {bar B}{sup 0} {yields} D*{sup +} {tau}{sup -}{bar {nu}}{sub {tau}}, which are sensitive to non-Standard Model amplitudes in certain scenarios. The data sample consists of 232 x 10{sup 6} {Upsilon}(4S) {yields} B{bar B} decays collected with the BABAR detector at the PEP-II e{sup +}e{sup -} collider. They select events with a D or D* meson and a light lepton ({ell} = e or {mu}) recoiling against a fully reconstructed B meson. They perform a fit to the joint distribution of lepton momentum and missing mass squared to distinguish signal B {yields} D{sup (*)}{tau}{sup -} {bar {nu}}{sub {tau}} ({tau}{sup -} {yields} {ell}{sup -} {bar {nu}}{sub {ell}}{nu}{sub {tau}}) events from the backgrounds, predominantly B {yields} D{sup (*)} {ell}{sup -}{bar {nu}}{sub {ell}}. They measure the branching-fraction ratios R(D) {triple_bond} {Beta}(B {yields} D{tau}{sup -} {bar {nu}}{sub {tau}})/{Beta}(B {yields} D{ell}{sup -} {bar {nu}}{sub {ell}}) and R(D*) {triple_bond} {Beta}(B {yields} D*{tau}{sup -} {bar {nu}}{sub {tau}})/{Beta}(B {yields} D* {ell}{sup -} {bar {nu}}{sub {ell}}) and, from a combined fit to B{sup -} and {bar B}{sup 0} channels, obtain the results R(D) = (41.6 {+-} 11.7 {+-} 5.2)% and R(D*) = (29.7 {+-} 5.6 {+-} 1.8)%, where the uncertainties are statistical and systematic. Normalizing to measured B{sup -} {yields} D{sup (*)0} {ell}{sup -} {bar {nu}}{sub {ell}} branching fractions, they obtain {Beta}(B {yields} D{tau}{sup -} {bar {nu}}{sub {tau}}) = (0.86 {+-} 0.24 {+-} 0.11 {+-} 0.06)% and {Beta}(B {yields} D*{tau}{sup -} {bar {nu}}{sub {tau}}) = (1.62 {+-} 0.31 {+-} 0.10 {+-} 0.05)%, where the additional third uncertainty is from the normalization mode. They also present, for the first time, distributions of the lepton momentum, |P*{sub {ell}}|, and the squared momentum transfer, q{sup 2}.

  19. Searches for Lepton Flavor Violation in the Decays tau+- ---> e+- gamma and tau+- ---> mu+- gamma

    SciTech Connect

    Aubert, Bernard; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, David Nathan; Hooberman, B.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; ,

    2010-06-11

    Searches for lepton-flavor-violating decays of a {tau} lepton to a lighter mass lepton and a photon have been performed with the entire dataset of (963 {+-} 7) x 10{sup 6} {tau} decays collected by the BABAR detector near the {Upsilon}(4S), {Upsilon}(3S) and {Upsilon}(2S) resonances. The searches yield no evidence of signals and they set upper limits on the branching fractions of {Beta}({tau}{sup {+-}} {yields} e{sup {+-}}{gamma}) < 3.3 x 10{sup -8} and {Beta}({tau}{sup {+-}} {yields} {mu}{sup {+-}}{gamma}) < 4.4 x 10{sup -8} at 90% confidence level.

  20. Search for tau decays to the eta meson

    SciTech Connect

    Skwarnicki, T.

    1987-12-01

    Using a sample of 530,000 tau leptons collected by the Crystal Ball experiment at the e/sup +/e/sup -/ storage ring DORIS II, we have searched for tau decays to the eta meson. No eta signal is found in the inclusive analysis, tau ..-->.. eta X, of 1-prong decays, leading to the upper limits, BR(tau/sup -/ ..-->.. nu ..pi../sup -/eta) <0.3%, BR(tau/sup -/ ..-->.. ..pi../sup -/..pi../sup 0/eta) <0.9%, BR(tau/sup -/ ..-->.. nu ..pi../sup -/..pi../sup 0/..pi../sup 0/eta) <3.1%, BR(tau/sup -/ ..-->.. nu ..pi../sup -/eta eta) <2.5% (95% CL). The decays, tau/sup -/ ..-->.. nu ..pi../sup -/eta and tau/sup -/ ..-->.. nu ..pi../sup -/..pi../sup 0/eta, are also not found in the exclusive analyses, while BR(tau/sup -/ ..-->.. nu ..pi../sup -/..pi../sup 0/) = (22.7 +- 0.9 +- 3.0)% and BR(tau/sup -/ ..-->.. nu ..pi../sup -/..pi../sup 0/..pi../sup 0/) = (7.0 +- 0.7 +- 1.4)% are measured in accord with the expectations. The hadronic final state, ..pi../sup -/..pi../sup 0/..pi../sup 0/, is reconstructed in tau decays for the first time. The results are preliminary. 21 refs., 10 figs.

  1. Hadronic decays of the tau lepton : {tau}- {yields} ({pi}{pi}{pi})- {nu}{tau} within Resonance Chiral Theory

    SciTech Connect

    Gomez Dumm, D.; Pich, A.; Portoles, J.

    2006-01-12

    {tau} decays into hadrons foresee the study of the hadronization of vector and axial-vector QCD currents, yielding relevant information on the dynamics of the resonances entering into the processes. We analyse {tau} {yields} {pi}{pi}{pi}{nu}{tau} decays within the framework of the Resonance Chiral Theory, comparing this theoretical scheme with the experimental data, namely ALEPH spectral function and branching ratio. Hence we get values for the mass and on-shell width of the a 1 (1260) resonance, and provide the structure functions that have been measured by OPAL and CLEO-II.

  2. Constraining new interactions with leptonic {tau} decays

    SciTech Connect

    Pich, A.; Silva, J.P.

    1995-10-01

    The recent measurements of the Michel parameters in {tau} decays enable, for the first time, a thorough analysis of the leptonic sector. In general, in models beyond the standard model, these parameters will be altered through changes in the {ital W} and {ital Z} couplings, and/or through interactions mediated by new gauge bosons. We perform a complete, model-independent analysis of the constraints imposed by the present data on such boson-mediated interactions, and point out the existence of useful relations among the couplings.

  3. Measurements of tau decays to three pions

    NASA Astrophysics Data System (ADS)

    Band, H. R.; Camporesi, T.; Chadwick, G. B.; Delfino, M. C.; De Sangro, R.; Ford, W. T.; Gettner, M. W.; Goderre, G. P.; Groom, D. E.; Hurst, R. B.; Johnson, J. R.; Lavine, T. L.; Leedy, R. E.; Maruyama, T.; Messner, R. L.; Moss, L. J.; Muller, F.; Nelson, H. N.; Peruzzi, I.; Piccolo, M.; Prepost, R.; Pyrlik, J.; Qi, N.; Read, A. L.; Ritson, D. M.; Rosenberg, L. J.; Sleeman, J. C.; Smith, J. G.; Venuti, J. P.; Verdini, P. G.; Von Goeler, E.; Weinstein, Roy; Wiser, D. E.; Zdarko, R. W.; MAC Collaboration

    1987-11-01

    We reports the result of a study of a tau decays with three pions in the final state ( ?? ??+?-?? and ?? ??0?0??) from data accumulated with the MAC detector operating at the PEP storage ring. The branching fractions for these modes are measured to be 0.0700.0030.007 and, with assumptions discussed in the text, 0.0870.0040.011, respectively. Assuming that these final states result from the decay of the a 1 meson, we measure the resonant parameters of the a 1 with the three charged pion sample to be ma1=11661811 MeV and ?a1=4057525 MeV, and with the one charged plus two neutral pions sample to be ma1=11644123 MeV and ?a1=41910857 MeV.

  4. A Search for Neutrinoless Tau Decays to Three Leptons

    SciTech Connect

    Kolb, Jeffrey A.; ,

    2008-09-24

    Using approximately 350 million {tau}{sup +}{tau}{sup -} pair events recorded with the BaBar detector at the Stanford Linear Accelerator Center between 1999 and 2006, a search has been made for neutrinoless, lepton-flavor violating tau decays to three lighter leptons. All six decay modes consistent with conservation of electric charge and energy have been considered. With signal selection efficiencies of 5-12%, we obtain 90% confidence level upper limits on the branching fraction {Beta}({tau} {yields} {ell}{ell}{ell}) in the range (4-8) x 10{sup -8}.

  5. Search for the Decay B+-->K+ tau-/+ mu+/-.

    PubMed

    Aubert, B; Bona, M; Boutigny, D; Karyotakis, Y; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Grauges, E; Lopez, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabe, T; Wenzel, W A; del Amo Sanchez, P; Hawkes, C M; Watson, A T; Held, T; Koch, H; Pelizaeus, M; Schroeder, T; Steinke, M; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Liu, F; Long, O; Shen, B C; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Panduro Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; Mclachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, G; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; LoSecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; de la Vaissire, Ch; Hamon, O; Leruste, Ph; Malcls, J; Ocariz, J; Perez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A

    2007-11-16

    We present a search for the lepton flavor violating decay B+-->K+ tau-/+ mu+/- using 383 x 10;{6} BB[over ] events collected by the BABAR experiment. The branching fraction for this decay can be substantially enhanced in new physics models. The kinematics of the tau from the signal B decay are inferred from the K+, mu, and other B in the event, which is fully reconstructed in one of a variety of hadronic decay modes, allowing the signal B candidate to be fully reconstructed. We observe no excess of events over the expected background and set a limit of B(B+-->K+ tau mu)<7.7 x 10(-5) at 90% confidence level, where the branching fraction is for the sum of the K+ tau- mu+ and K+ tau+mu- final states. We use this result to improve a model-independent bound on the energy scale of flavor-changing new physics. PMID:18233132

  6. The decay tau. -->. rho nu (and rho. -->. pi. eta nu. )

    SciTech Connect

    Stockhausen, W.

    1987-04-01

    Motivated by the question of missing exclusive branching fractions in tau decays, mostly suspected to be in one prong decays with neutrals, we have studied the decay tau ..-->.. rho nu in tau pair production by e/sup +/e/sup -/ annihilation at ..sqrt..s = 3.77 GeV. The branching fraction is measured to be B(tau ..-->.. rho nu) = (23.0 +- 1.3 +- 1.7)% consistent with known measurements and not offering a solution to the branching ratio question. No eta signal in the ..gamma gamma.. mass spectrum pointing to a decay tau ..-->.. eta ..pi.. nu is obvious. An upper limit on this branching fraction is given.

  7. CP Violation in Tau to K* Decays

    SciTech Connect

    Hodgkinson, Mark; /Manchester U.

    2006-03-10

    A sample of {tau}{sup {+-}} {yields} K*{sup {+-}} decays with K*{sup {+-}} {yields} K{sub S}{sup 0}{pi}{sup {+-}} and K{sub S}{sup 0} {yields} {pi}{sup +}{pi}{sup -}, using 123.4 fb{sup -1} of data collected by the BaBar detector at the Stanford Linear Accelerator Center, is used to search for a direct CP violation effect in the charged Higgs sector. No evidence of CP violation is found and the imaginary part of the charged Higgs coupling, {l_brace}Im{r_brace}({Lambda}), in the Multi-Higgs-Doublet-Model is found to be at -0.284 < {l_brace}Im{r_brace}({Lambda}) < 0.200 at 90% Confidence Level. In addition the installation of the kk2f Monte Carlo generator into the BaBar software framework is described.

  8. Multiple-neutral-meson decays of the /tau/ lepton and electromagnetic calorimeter requirements at Tau-Charm Factory

    SciTech Connect

    Gan, K.K.

    1989-08-01

    This is a study of the physics sensitivity to the multiple-neutral-meson decays of the /tau/ lepton at the Tau-Charm Factory. The sensitivity is compared for a moderate and an ultimate electromagnetic calorimeter. With the high luminosity of the Tau- Charm Factory, a very large sample of the decays /tau//sup /minus// /yields/ /pi//sup /minus//2/pi//sup 0//nu//sub /tau// and /tau//sup /minus// /yields/ /pi//sup /minus//3/pi//sup 0//nu//sub /tau// can be collected with both detectors. However, with the ultimate detector, 2/pi//sup 0/ and 3/pi//sup 0/ can be unambiguously reconstructed with very little background. For the suppressed decay /tau//sup /minus// /yields/ /pi//sup /minus///eta//pi//sup 0//nu//sub /tau//, only the ultimate detector has the sensitivity. The ultimate detector is also sensitive to the more suppressed decay /tau//sup /minus// /yields/ K/sup /minus///eta//nu//sub /tau// and the moderate detector may have the sensitivity if the hadronic background is not significantly larger than that predicted by Lund. In the case of the highly suppressed second-class-current decay /tau//sup /minus// /yields/ /pi//sup /minus///eta//nu//sub /tau//, only the ultimate detector has sensitivity. The sensitivity can be greatly enhanced with a small-angle photon veto. 16 refs., 9 figs., 2 tabs.

  9. Higgs mediated lepton flavor violating tau decays {tau}{yields}{mu}{gamma} and {tau}{yields}{mu}{gamma}{gamma} in effective theories

    SciTech Connect

    Aranda, J. I.; Tututi, E. S.; Toscano, J. J.

    2008-07-01

    The size of the branching ratios for the {tau}{yields}{mu}{gamma} and {tau}{yields}{mu}{gamma}{gamma} decays induced by a lepton flavor violating Higgs interaction H{tau}{mu} is studied in the framework of effective field theories. The best constraint on the H{tau}{mu} vertex, derived from the know measurement on the muon anomalous magnetic moment, is used to impose the upper bounds Br({tau}{yields}{mu}{gamma})<7.5x10{sup -10} and Br({tau}{yields}{mu}{gamma}{gamma})<2.3x10{sup -12}, which are more stringent than current experimental limits on this class of transitions.

  10. ({omega},{phi})P{sup -} decays of tau leptons

    SciTech Connect

    Flores-Tlalpa, A.; Castro, G. Lopez

    2008-06-01

    The {tau}{sup -}{yields}({omega},{phi})P{sup -}{nu}{sub {tau}} decays, where P{sup -}={pi}{sup -} or K{sup -}, are considered within a phenomenological model with dominance of meson intermediate states. We assume SU(3) flavor symmetry to fix some of the unknown strong interaction couplings. Our predictions for the {tau}{sup -}{yields}{phi}({pi}{sup -},K{sup -}){nu}{sub {tau}} branching fractions are in good agreement with recent measurements of the BABAR and BELLE Collaborations.

  11. The decay. tau. sup minus r arrow K sup minus K sup +. pi. sup minus. nu. sub. tau. and the. nu. sub. tau. mass

    SciTech Connect

    Gomez-Cadenas, J.J. ); Gonzalez-Garcia, M.C.; Pich, A. Instituto de Fisica Corpuscular, Consejo Superior de Investigaciones Cientificas, Universidad de Valencia, Burjasot )

    1990-11-01

    In this paper, we present a model based on the effective chiral Lagrangian to describe the decay {tau}{sup {minus}}{r arrow}{ital K}{sup {minus}}{ital K}{sup +}{pi}{sup {minus}}{nu}{sub {tau}}. Using our model we study the possible limits on the {nu}{sub {tau}} mass that can be achieved by a high-statistics, high-precision experiment taking data close to the {tau}-pair production threshold.

  12. Higgs Boson decay to Tau Pairs at the CMS Experiment

    NASA Astrophysics Data System (ADS)

    Choudhury, Somnath

    2015-03-01

    The results on the standard model Higgs boson in tau pair decay using 25 fb-1 of pp collision data at 7 and 8 TeV center-of-mass energies collected by the CMS detector at the LHC has been presented. A direct evidence of the Higgs-lepton coupling is established with the tau pair decay mode. Searches for Higgs bosons decaying to tau leptons in scenarios beyond the standard model such as supersymmetry within the minimal extension of the model has also been reported.

  13. Study of the Tau- to Pi- Pi+ Pi- Pi0 Nu/Tau And Tau- to Pi- Pi- Pi+ Eta Nu/Tau Decays Using the BaBar Detector

    SciTech Connect

    Sobie, Randall; /Victoria U.

    2007-11-14

    The {tau}{sup -} {yields} {pi}{sup -}{pi}{sup +}{pi}{sup -}{nu}{sub {tau}} and {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{eta}{nu}{sub {tau}} decays have been studied with the BABAR detector. Preliminary branching fractions on the two modes are presented. The {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{eta}{nu}{sub {tau}} mode is found to have a large contribution from the {tau}{sup -} {yields} {omega}{pi}{sup -}{nu}{sub {tau}} decay. The {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{eta}{nu}{sub {tau}} decay is studied using the {eta} {yields} {gamma}{gamma} mode and the {tau}{sup -} f{sub 1}(1285){pi}{sup -}{nu}{sub {tau}} decay is seen to be the primary source of these decays. A 90% confidence level upper limit is placed on the {tau}{sup -} {yields} {eta}{prime}(958){pi}{sup -}{nu}{sub {tau}} decay which proceeds through a second-class current and is expected to be forbidden in the limit of perfect isospin symmetry.

  14. The strong coupling from tau decays without prejudice

    NASA Astrophysics Data System (ADS)

    Boito, Diogo; Golterman, Maarten; Jamin, Matthias; Mahdavi, Andisheh; Maltman, Kim; Osborne, James; Peris, Santiago

    2014-08-01

    We review our recent determination of the strong coupling ?s from the OPAL data for non-strange hadronic tau decays. We find that ?s (m?2)= 0.325 0.018 using fixed-order perturbation theory, and ?s (m?2)= 0.347 0.025 using contour-improved perturbation theory. At present, these values supersede any earlier determinations of the strong coupling from hadronic tau decays, including those from ALEPH data.

  15. Lepton-Flavor-Violating Tau Decays at BaBar

    SciTech Connect

    Marchiori, G.; /Paris, LPTHE

    2012-04-09

    We present the most recent searches for lepton-flavor-violating (LFV) {tau} decays in BABAR. We find no evidence of {tau} decaying to three charged leptons or to a charged lepton and a neutral meson (K{sub S}{sup 0}, {rho}, {phi}, K*{sup 0}, {bar K}*{sup 0}), and set upper limits on the corresponding branching fractions (BF) between 1.8 and 19 x 10{sup -8} at 90% confidence level (CL).

  16. Sensitivity to the Higgs sector of SUSY-seesaw models via LFV tau decays

    SciTech Connect

    Herrero, M.; Rodriguez-Sanchez, A.

    2010-02-10

    Here we study and compare the sensitivity to the Higgs sector of SUSY-seesaw models via the LFV tau decays: tau->3mu, tau->muK{sup +}K{sup -}, tau->mueta and tau->mu f{sub 0}. We emphasize that, at present, the two latter channels are the most efficient ones to test indirectly the Higgs particles.

  17. Resonance Effective Theory Approach to {tau} {yields} 3{pi}{nu}{tau} Decays

    SciTech Connect

    Gomez Dumm, D.; Pich, A.; Portoles, J.

    2004-12-02

    The decays {tau} {yields} 3{pi}{nu}{tau} are analyzed in the framework of the resonance effective theory of QCD, We derive the effective chiral Lagrangian relevant for the evaluation of the hadronic axial-vector current, taking into account the constraints imposed by QCD on the high energy asymptotic behaviour. Then we fit the unknown parameters to the spectral function and branching ratio measured by ALEPH, showing that the theory is in good agreement with experimental data. A detailed description of the work sketched here can be found.

  18. Search for lepton flavor violating decays tau+/--->l+/-omega.

    PubMed

    Aubert, B; Bona, M; Karyotakis, Y; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Grauges, E; Lopez, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes Pegna, D; Lynch, G; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabe, T; Wenzel, W A; Del Amo Sanchez, P; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Buzykaev, A R; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Gary, J W; Liu, F; Long, O; Shen, B C; Vitug, G M; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Echenard, B; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Ayad, R; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Nash, J A; Panduro Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, G; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; Losecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Sekula, S J; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; de la Vaissire, Ch; Hamon, O; Leruste, Ph; Malcls, J; Ocariz, J; Perez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Biesiada, J; Lau, Y P; Lu, C; Olsen, J

    2008-02-22

    A search for lepton flavor violating decays of a tau to a lighter-mass charged lepton and an omega vector meson is performed using 384.1 fb(-1) of e(+)e(-) annihilation data collected with the BABAR detector at the Stanford Linear Accelerator Center PEP-II storage ring. No signal is found, and the upper limits on the branching ratios are determined to be B(tau(+/-)-->e;{+/-}omega)<1.1 x10 (-7) and B(tau(+/-)-->micro(+/-)omega)<1.0 x 10(-7) at 90% confidence level. PMID:18352541

  19. Search for tau- ---> 4pi- 3pi+ (pi0) nu/tau Decays

    SciTech Connect

    Ter-Antonian, R.; Kass, R.; Allmendinger, T.; Hast, C.; /SLAC

    2005-06-21

    A search for the decay of the {tau} lepton to seven charged pions and at most one {pi}{sup 0} was performed using the BABAR detector at the PEP-II e{sup +}e{sup -} collider. The analysis uses data recorded on and near the {Upsilon}(4S) resonance between 1999 and 2003, a total of 124.3 fb{sup -1}. They observe 7 events with an expected background of 11.9 {+-} 2.2 events and calculate a preliminary upper limit of BR({tau}{sup -} {yields} 4{pi}{sup -} 3{pi}{sup +}({pi}{sup 0}){nu}{sub {tau}}) < 2.7 x 10{sup -7} at 90% CL. This is a significant improvement over the previous limit established by the CLEO Collaboration.

  20. Lepton Flavour Violation in Tau Decays at BaBar

    SciTech Connect

    Wilson, F.F.; /Rutherford

    2011-11-07

    Recent results from {tau} physics studies at BABAR are presented with an emphasis on Lepton Flavour Violation measurements. The results from the current generation of B-meson Factories are already beginning to constrain the parameter space of models that go beyond the Standard Model. By the end of their data-taking, the current generation of B-meson factories will have produced nearly 2 billion {tau} pair decays. The physics potential of this legacy has only just begun to be exploited.

  1. Study of the tau- ---> pi- pi- pi+ pi0 pi0 nu/tau and tau- --> 3h- 2h+ nu/tau Decays Using the BaBar Detector

    SciTech Connect

    Sobie, R.; /Victoria U.

    2005-06-21

    The {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}} and {tau}{sup -} {yields} 3h{sup -} 2h{sup +} {nu}{sub {tau}} decays have been studied using the BABAR experiment at the PEP-II e{sup +}e{sup -} storage ring. Preliminary branching fractions are given for the {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}} and to the sub-channels {tau}{sup -} {yields} {eta}{pi}{sup -} {pi}{sup 0}{nu}{sub {tau}} and {tau}{sup -} {yields} {omega}(782){pi}{sup -}{pi}{sup 0}{nu}{sub {tau}}. A preliminary upper limit is given on the branching fraction for the {phi}(1020){pi}{sup -}{pi}{sup 0}{nu}{sub {tau}} mode. In addition a preliminary measurement of the branching fraction of the {tau}{sup -} {yields} 3h{sup -}2h{sup +} {nu}{sub {tau}} decay (h = {pi}, K) is presented.

  2. Searches for Lepton flavor violation in the decays tau{+/-}-->e{+/-}gamma and tau{+/-}-->mu{+/-}gamma.

    PubMed

    Aubert, B; Karyotakis, Y; Lees, J P; Poireau, V; Prencipe, E; Prudent, X; Tisserand, V; Garra Tico, J; Grauges, E; Martinelli, M; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Battaglia, M; Brown, D N; Hooberman, B; Kerth, L T; Kolomensky, Yu G; Lynch, G; Osipenkov, I L; Tackmann, K; Tanabe, T; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Asgeirsson, D J; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Randle-Conde, A; Blinov, V E; Bukin, A D; Buzykaev, A R; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Atmacan, H; Gary, J W; Liu, F; Long, O; Vitug, G M; Yasin, Z; Sharma, V; Campagnari, C; Hong, T M; Kovalskyi, D; Mazur, M A; Richman, J D; Beck, T W; Eisner, A M; Heusch, C A; Kroseberg, J; Lockman, W S; Martinez, A J; Schalk, T; Schumm, B A; Seiden, A; Wang, L; Winstrom, L O; Cheng, C H; Doll, D A; Echenard, B; Fang, F; Hitlin, D G; Narsky, I; Ongmongkolkul, P; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Bloom, P C; Ford, W T; Gaz, A; Hirschauer, J F; Nagel, M; Nauenberg, U; Smith, J G; Wagner, S R; Ayad, R; Toki, W H; Feltresi, E; Hauke, A; Jasper, H; Karbach, T M; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Kobel, M J; Nogowski, R; Schubert, K R; Schwierz, R; Bernard, D; Latour, E; Verderi, M; Clark, P J; Playfer, S; Watson, J E; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Fioravanti, E; Franchini, P; Luppi, E; Munerato, M; Negrini, M; Petrella, A; Piemontese, L; Santoro, V; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Contri, R; Guido, E; Lo Vetere, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Tosi, S; Morii, M; Adametz, A; Marks, J; Schenk, S; Uwer, U; Bernlochner, F U; Lacker, H M; Lueck, T; Volk, A; Dauncey, P D; Tibbetts, M; Behera, P K; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Arnaud, N; D'Orazio, A; Davier, M; Derkach, D; Firmino da Costa, J; Grosdidier, G; Le Diberder, F; Lepeltier, V; Lutz, A M; Malaescu, B; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Touramanis, C; Bevan, A J; Clarke, C K; Di Lodovico, F; Sacco, R; Sigamani, M; Cowan, G; Paramesvaran, S; Wren, A C; Brown, D N; Davis, C L; Denig, A G; Fritsch, M; Gradl, W; Hafner, A; Alwyn, K E; Bailey, D; Barlow, R J; Jackson, G; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Dallapiccola, C; Salvati, E; Cowan, R; Dujmic, D; Fisher, P H; Henderson, S W; Sciolla, G; Spitznagel, M; Yamamoto, R K; Zhao, M; Patel, P M; Robertson, S H; Schram, M; Biassoni, P; Lazzaro, A; Lombardo, V; Palombo, F; Stracka, S; Cremaldi, L; Godang, R; Kroeger, R; Sonnek, P; Summers, D J; Zhao, H W; Nguyen, X; Simard, M; Taras, P; Nicholson, H; De Nardo, G; Lista, L; Monorchio, D; Onorato, G; Sciacca, C; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; Losecco, J M; Wang, W F; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Sekula, S J; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Castelli, G; Gagliardi, N; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Del Amo Sanchez, P; Ben-Haim, E; Bonneaud, G R; Briand, H; Chauveau, J; Hamon, O; Leruste, Ph; Marchiori, G; Ocariz, J; Perez, A; Prendki, J; Sitt, S; Gladney, L; Biasini, M; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Calderini, G; Carpinelli, M; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J J; Lopes Pegna, D; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Anulli, F; Baracchini, E; Cavoto, G; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schrder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Wilson, F F; Emery, S; Esteve, L; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yche, Ch; Zito, M; Allen, M T; Aston, D; Bard, D J; Bartoldus, R; Benitez, J F; Cenci, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Franco Sevilla, M; Fulsom, B G; Gabareen, A M; Graham, M T; Grenier, P; Hast, C; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Lindquist, B; Luitz, S; Luth, V; Lynch, H L; Macfarlane, D B

    2010-01-15

    Searches for lepton-flavor-violating decays of a tau lepton to a lighter mass lepton and a photon have been performed with the entire data set of (963+/-7)x10{6} tau decays collected by the BABAR detector near the Upsilon(4S), Upsilon(3S) and Upsilon(2S) resonances. The searches yield no evidence of signals and we set upper limits on the branching fractions of B(tau{+/-}-->e{+/-}gamma)<3.3x10{-8} and B(tau{+/-}-->mu{+/-}gamma)<4.4x10{-8} at 90% confidence level. PMID:20366586

  3. Measurement of the absolute branching fraction of Ds+ --> tau+ nutau decay.

    PubMed

    Ecklund, K M; Love, W; Savinov, V; Lopez, A; Mendez, H; Ramirez, J; Ge, J Y; Miller, D H; Shipsey, I P J; Xin, B; Adams, G S; Anderson, M; Cummings, J P; Danko, I; Hu, D; Moziak, B; Napolitano, J; He, Q; Insler, J; Muramatsu, H; Park, C S; Thorndike, E H; Yang, F; Artuso, M; Blusk, S; Khalil, S; Li, J; Mountain, R; Nisar, S; Randrianarivony, K; Sultana, N; Skwarnicki, T; Stone, S; Wang, J C; Zhang, L M; Bonvicini, G; Cinabro, D; Dubrovin, M; Lincoln, A; Rademacker, J; Asner, D M; Edwards, K W; Naik, P; Reed, J; Briere, R A; Ferguson, T; Tatishvili, G; Vogel, H; Watkins, M E; Rosner, J L; Alexander, J P; Cassel, D G; Duboscq, J E; Ehrlich, R; Fields, L; Gibbons, L; Gray, R; Gray, S W; Hartill, D L; Heltsley, B K; Hertz, D; Jones, C D; Kandaswamy, J; Kreinick, D L; Kuznetsov, V E; Mahlke-Krüger, H; Mohapatra, D; Onyisi, P U E; Patterson, J R; Peterson, D; Riley, D; Ryd, A; Sadoff, A J; Shi, X; Stroiney, S; Sun, W M; Wilksen, T; Athar, S B; Patel, R; Yelton, J; Rubin, P; Eisenstein, B I; Karliner, I; Mehrabyan, S; Lowrey, N; Selen, M; White, E J; Wiss, J; Mitchell, R E; Shepherd, M R; Besson, D; Pedlar, T K; Cronin-Hennessy, D; Gao, K Y; Hietala, J; Kubota, Y; Klein, T; Lang, B W; Poling, R; Scott, A W; Zweber, P; Dobbs, S; Metreveli, Z; Seth, K K; Tomaradze, A; Libby, J; Powell, A; Wilkinson, G

    2008-04-25

    Using a sample of tagged D(s)(+) decays collected near the D(s)(*+/-)D(s)(-/+) peak production energy in e(+)e(-) collisions with the CLEO-c detector, we study the leptonic decay D(s)(+)-->tau(+)nu(tau) via the decay channel tau(+)-->e(+)nu(e)nu(tau). We measure B(D(s)(+)-->tau(+)nu(tau))=(6.17+/-0.71+/-0.34)%, where the first error is statistical and the second systematic. Combining this result with our measurements of D(s)(+)-->mu(+)nu(mu) and D(s)(+)-->tau(+)nu(tau) (via tau(+)-->pi(+)nu(tau)), we determine f(D(s))=(274+/-10+/-5) MeV. PMID:18518183

  4. Study of High-multiplicity 3-prong and 5-prong Tau Decays at BaBar

    SciTech Connect

    Lees, J.P

    2012-06-01

    We present measurements of the branching fractions of 3-prong and 5-prong {tau} decay modes using a sample of 430 million {tau} lepton pairs, corresponding to an integrated luminosity of 468 fb{sup -1}, collected with the BABAR detector at the PEP-II asymmetric energy e{sup +}e{sup -} storage rings. The {tau}{sup -} {yields} (3{pi}){sup -} {eta}{nu}{sub {tau}}, {tau}{sup -} {yields} (3{pi}){sup -} {yields} {omega}{nu}{sub {tau}} and {tau}{sup -} {yields} {pi}{sup -} f{sub 1}(1285){nu}{sub {tau}} branching fractions are presented as well as a new limit on the branching fraction of the isospin-forbidden, second-class current {tau}{sup -} {yields} {pi}{sup -} {eta}{prime}(958){nu}{sub {tau}} decay. We find no evidence for charged kaons in these decay modes and place the first upper limits on their branching fractions.

  5. Hadron structure in {tau}{yields}KK{pi}{nu}{sub {tau}}decays

    SciTech Connect

    Gomez Dumm, D.; Roig, P.; Pich, A.; Portoles, J.

    2010-02-01

    We analyze the hadronization structure of both vector and axial-vector currents leading to {tau}{yields}KK{pi}{nu}{sub {tau}}decays. At leading order in the 1/N{sub C} expansion, and considering only the contribution of the lightest resonances, we work out, within the framework of the resonance chiral Lagrangian, the structure of the local vertices involved in those processes. The couplings in the resonance theory are constrained by imposing the asymptotic behavior of vector and axial-vector spectral functions ruled by QCD. In this way we predict the hadron spectra and conclude that, contrary to previous assertions, the vector contribution dominates by far over the axial-vector one in all KK{pi} charge channels.

  6. Lepton Universality, |V(Us)| and Search for Second Class Current in Tau Decays

    SciTech Connect

    Banerjee, Swagato; /Victoria U.

    2011-11-10

    Several hundred million {tau} decays have been studied with the BABAR detector at the PEP-II e{sup +}e{sup -} collider at the SLAC National Accelerator Laboratory. Recent results on Charged Current Lepton Universality and two independent measurements of |V{sub us}| using {tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}, {mu}{sup -}{bar {nu}}{sub {mu}}{nu}{sub {tau}}, {pi}{sup -}{nu}{sub {tau}}, K{sup -} {nu}{sub {tau}} and K{sub S}{sup 0}{pi}{sup -} {nu}{sub {tau}} decays, and a search for Second Class Current in {tau}{sup -} {yields} {pi}{sup -} {omega}{nu}{sub {tau}} decays are presented, where the charge conjugate decay modes are also implied.

  7. Search for CP Violation in the Decay tau- \\to pi- K^0_S (>= 0 pi0) nu_tau

    SciTech Connect

    Lees, J.P.; Poireau, V.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Milanes, D.A.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Koch, H.; Schroeder, T.; Asgeirsson, D.J.; Hearty, C.; Mattison, T.S.; McKenna, J.A.; /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /Indian Inst. Tech., Guwahati /Harvard U. /Harvey Mudd Coll. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Paris U., VI-VII /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /INFN, Naples /Naples U. /NIKHEF, Amsterdam /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /Pisa U. /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Southern Methodist U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas Nuclear Corp., Austin /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2012-02-16

    We report a search for CP violation in the decay {tau}{sup -} {yields} {pi}{sup -}K{sub S}{sup 0}({>=} 0{pi}{sup 0}){nu}{sub {tau}} using a dataset of 437 million {tau} lepton pairs, corresponding to an integrated luminosity of 476 fb{sup -1}, collected with the BABAR detector at the PEP-II asymmetric energy e{sup +}e{sup -} storage rings. The CP-violating decay-rate asymmetry is determined to be (-0.45 {+-} 0.24 {+-} 0.11)%, approximately three standard deviations from the Standard Model prediction of (0.33 {+-} 0.01)%.

  8. Measurement of the tau- to eta pi-pi+pi-nu tau Branching Fraction and a Search for a Second-Class Current in the tau- to eta'(958)pi-nu tau Decay

    SciTech Connect

    Aubert, B.; Bona, M.; Boutigny, D.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prudent, X.; Tisserand, V.; Zghiche, A.; Garra Tico, J.; Grauges, E.; Lopez, L.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Abrams, G.S.; Battaglia, M.; Brown, David Nathan; Button-Shafer, J.; /LBL, Berkeley /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /Bristol U. /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /Ferrara U. /Frascati /Genoa U. /Harvard U. /Heidelberg U. /Imperial Coll., London /Iowa U. /Iowa State U. /Johns Hopkins U. /Karlsruhe U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT, LNS /McGill U. /Milan U. /INFN, Milan /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /Naples U. /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /Padua U. /Paris U., VI-VII /Pennsylvania U. /Perugia U. /Pisa U. /Princeton U. /INFN, Rome /Rostock U. /Rutherford /DSM, DAPNIA, Saclay /South Carolina U. /SLAC /Stanford U., Phys. Dept. /SUNY, Albany /Tennessee U. /Texas U. /Texas U., Dallas /Turin U. /INFN, Turin /Trieste U. /Valencia U., IFIC /Victoria U. /Warwick U. /Wisconsin U., Madison /Yale U.

    2008-03-24

    The {tau}{sup -} {yields} {eta}{pi}{sup -}{pi}{sup +}{pi}{sup -}{nu}{sub {tau}} decay with the {eta} {yields} {gamma}{gamma} mode is studied using 384 fb{sup -1} of data collected by the BABAR detector. The branching fraction is measured to be (1.60 {+-} 0.05 {+-} 0.11) x 10{sup -4}. It is found that {tau}{sup -} {yields} f{sub 1}(1285){pi}{sup -} {nu}{sub {tau}} {yields} {eta}{pi}{sup -}{pi}{sup +}{pi}{sup -}{nu}{sub {tau}} is the dominant decay mode with a branching fraction of (1.11 {+-} 0.06 {+-} 0.05) x 10{sup -4}. The first error on the branching fractions is statistical and the second systematic. In addition, a 90% confidence level upper limit on the branching fraction of the {tau}{sup -} {yields} {eta}{prime}(958){pi}{sup -}{nu}{sub {tau}} decay is measured to be 7.2 x 10{sup -6}. This last decay proceeds through a second-class current and is expected to be forbidden in the limit of isospin symmetry.

  9. Exclusive branching-fraction measurements of semileptonic tau decays into three charged hadrons, into phipi(-)nu tau, and into phi K(-)nu tau.

    PubMed

    Aubert, B; Bona, M; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Gill, M S; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Pegna, D Lopes; Lynch, G; Mir, L M; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; del Amo Sanchez, P; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Watson, A T; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Cottingham, W N; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Sherwood, D J; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Best, D S; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Roethel, W; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; Hadavand, H K; Hill, E J; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Cheng, C H; Dvoretskii, A; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Zeng, Q; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Brandt, T; Klose, V; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Lee, C L; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Nash, J A; Nikolich, M B; Vazquez, W Panduro; Behera, P K; Chai, X; Charles, M J; Mallik, U; Meyer, N T; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gritsan, A V; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Oyanguren, A; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; Clarke, C K; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Jackson, P S; McMahon, T R; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; Naisbit, M T; Williams, J C; Yi, J I; Chen, C; Hulsbergen, W D; Jawahery, A; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Saremi, S; Staengle, H; Cowan, R; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; LoSecco, J M; Benelli, G; Corwin, L A; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Rahimi, A M; Regensburger, J J; Ter-Antonyan, R; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Potter, C T; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H

    2008-01-11

    Using a data sample corresponding to an integrated luminosity of 342 fb(-1) collected with the BABAR detector at the SLAC PEP-II electron-positron storage ring operating at a center-of-mass energy near 10.58 GeV, we measure B(tau(-)--> pi(-)pi(-)pi+nu(tau)(ex.K(S0))=(8.83+/-0.01+/-0.13)%, B(tau(-) -->K(-)pi(-)pi+nu tau(ex.K(S0))=(0.273+/-0.002+/-0.009)%, B(tau(-) -->K(-)pi(-)K+nu tau)=(0.1346+/-0.0010+/-0.0036)%, and B(tau(-) -->K(-)K(-)K+nu tau)=(1.58+/-0.13+/-0.12)x10;{-5}, where the uncertainties are statistical and systematic, respectively. These include significant improvements over previous measurements and a first measurement of B(tau(-) -->K(-)K(-)K+nu tau) in which no resonance structure is assumed. We also report a first measurement of B(tau(-) -->var phi(-)nu tau)=(3.42+/-0.55+/-0.25)x10(-5), a new measurement of B(tau(-) -->var phi K(-)nu tau)=(3.39+/-0.20+/-0.28)x10(-5) and a first upper limit on B(tau(-) -->K(-)K(-)K+nu tau(ex.var phi)). PMID:18232752

  10. Tau Immunotherapy.

    PubMed

    Sigurdsson, Einar M

    2016-01-01

    In recent years, tau immunotherapy has advanced from proof-of-concept studies [Sigurdsson EM, NIH R01AG020197, 2001; Asuni AA, et al: J Neurosci 2007;27:9115-9129], which have now been confirmed and extended by us and others. Phase I clinical trials on active and passive tau immunizations are being conducted, with several additional passive tau antibody trials likely to be initiated in the near future for Alzheimer's disease and other tauopathies. Because tau pathology correlates better with the degree of dementia than amyloid-? (A?) pathology, greater clinical efficacy may be achieved by clearing tau than A? aggregates in the later stages of the disease, when cognitive impairments become evident. Substantial insight has now been obtained regarding which epitopes to target, mechanism of action and potential toxicity, but much remains to be clarified. All of these factors likely depend on the model/disease or stage of pathology and the immunogen/antibody. Interestingly, tau antibodies interact with the protein both extra- and intracellularly, but the importance of each site for tau clearance is not well defined. Some antibodies are readily taken up into neurons, whereas others are not. It can be argued that extracellular clearance may be safer but less efficacious than intraneuronal clearance and/or sequestration to prevent secretion and further spread of tau pathology. Development of therapeutic tau antibodies has led to antibody-derived imaging probes, which are more specific than the dye-based compounds that are already in clinical trials. Such specificity may give valuable information on the pathological tau epitope profile, which could then guide the selection of therapeutic antibodies for maximal efficacy and safety. Hopefully, tau immunotherapy will be effective in clinical trials, and further advanced by mechanistic clarification in experimental models with insights from biomarkers and postmortem analyses of clinical subjects. PMID:26551002

  11. Measurement of sigma(ppbar->Z) Br(Z->tau+tau-) and search for Higgs bosons decaying to tau+tau- at s**(1/2) = 1.96 TeV

    SciTech Connect

    Galea, Cristina Florina; /Nijmegen U.

    2008-01-01

    The resonant production of tau-lepton pairs is as interesting for the study of Standard Model (SM) physics as the production of lighter leptons pairs. For new phenomena, such as Higgs boson production or in case new particles beyond the SM would arise, the detection of (resonant) pairs of tau leptons becomes much more interesting. This is due to the fact that tau leptons are much heavier than the other leptons, which increases the chance that these new phenomena would be observed first in this channel. Unfortunately their clean detection is far more difficult than that of muons or electrons. The cross section times branching ratio {sigma}{center_dot} Br for the process p{bar p} {yields} Z {yields} {tau}{sup +}{tau}{sup -} was measured at {radical}s = 1.96 GeV using 1.0 fb{sup -1} of data collected by the D0 experiment. This measurement was performed in the channel in which one of the tau leptons decays to a muon and neutrinos, while the other decays either hadronically or to an electron and neutrinos. A set of 1511 events, of which about 20% estimated background, passed all selection criteria. The trigger and muon reconstruction efficiencies, as well as the efficiency for track reconstruction were obtained from data using the 'tag and probe' method on Z {yields} {mu}{sup +}{mu}{sup -} events. The multijet background was estimated from the sample of events which passed all selection criteria but in which the muon and the tau candidate had the same charge. The W {yields} {mu}{nu} + jets background was modeled by Monte Carlo simulations, but normalized to data. All the other backgrounds, as well as the efficiency for Z {yields} {tau}{sup +}{tau}{sup -} events were estimated using simulated events normalized to the theoretical calculations of cross sections at next-to-leading order or next-to-next-to-leading order. The energy of the tau candidates was corrected for the estimated response of the charged pions in the calorimeter, which is of the order 50-80%. Since the charged pion response in data was not well reproduced by the default simulation of hadronic interactions (Geisha), a different simulation (gCALOR) was used to obtain an estimated charged pion response consistent with the one measured in data. This tau energy correction method makes use of the superior resolution of the track momentum measurement compared to the resolution of the tau candidate energy as measured by the calorimeter, which leads to a better data--simulation agreement and a decrease of 10% in the resolution of the visible mass peak. The result of this measurement is {sigma}(p{bar p} {yields} Z) {center_dot} Br(Z {yields} {tau}{sup +}{tau}{sup -}) = 240 {+-} 8(stat) {+-} 12(syst) {+-} 15(lumi) pb, in good agreement with the theoretical predictions of 241.6{sub -3.2}{sup +3.6} pb [79] or 251.9{sub -12}{sup +5.1} pb [93-95], as well as with other measurements performed by the D0 and CDF experiments in all channels in which the Z boson decays leptonically [96-100]. This is the most precise Z boson cross section measurement to date performed in the tau lepton channel at hadron colliders. The analysis demonstrates the ability of the D0 experiment to identify tau leptons decaying hadronically with good efficiency and high purity, a challenging task in p{bar p} collisions where the number of jets resembling tau leptons is very high. This achievement forms a solid basis for other analyses using hadronic tau lepton decays, such as the search for the Higgs boson decaying into tau-lepton pairs, which was performed for the last part of this thesis.

  12. Measurement of Cabibbo-Suppressed Tau Lepton Decays and the Determination of |Vus|

    SciTech Connect

    Schenk, Stefan; /SLAC

    2008-12-16

    This work presents simultaneous branching fraction measurements of the decay modes {tau}{sup -} {yields} K{sup -} n{pi}{sup 0}{nu}{sub {tau}} with n = 0,1,2,3 and {tau}{sup -} {yields} {pi}{sup -} n{pi}{sup 0}{nu}{sub {tau}} with n = 3,4. The analysis is based on a data sample of 427 x 10{sup 6} {tau}{sup +}{tau}{sup -} pairs recorded with the BABAR detector, which corresponds to an integrated luminosity of 464.4 fb{sup -1}. The measured values are {Beta}({tau}{sup -} {yields} K{sup -}{nu}{sub {tau}}) = (6.57 {+-} 0.03 {+-} 0.11) x 10{sup -3}, {Beta}({tau}{sup -} {yields} K{sup -}{pi}{sup 0}{nu}{sub {tau}}) = (4.61 {+-} 0.03 {+-} 0.11) x 10{sup -3}, {Beta}({tau}{sup -} {yields} K{sup -} {pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}}) = (5.05 {+-} 0.17 {+-} 0.44) x 10{sup -4}, {Beta}({tau}{sup -} {yields} K{sup -}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}}) = (1.31 {+-} 0.43 {+-} 0.40) x 10{sup -4}, {Beta}({tau}{sup 0} {yields} {pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}}) = (1.263 {+-} 0.008 {+-} 0.078) x 10{sup -2} and {Beta}({tau}{sup 0} {yields} {pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}}) = (9.6 {+-} 0.5 {+-} 1.2) x 10{sup -4}, where the uncertainties are statistical and systematic, respectively. All measurements are compatible with the current world averages whereas the uncertainties are significantly smaller by a factor of up to five. The determination of {Beta}({tau}{sup 0} {yields} {pi}{sup -}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{pi}{sup 0}{nu}{sub {tau}}) is the first measurement of this branching fraction. The measured branching fractions are combined with the current world averages. Using the new averages, an updated determination of |V{sub us}| from hadronic {tau} decays yields |V{sub us}| = 0.2146 {+-} 0.0025, which improves previous measurements by 19%. Its uncertainty is comparable to the one of the current world average from semileptonic kaon decays.

  13. Measurements of Charged Current Lepton Universality and |V{sub us}| Using Tau Lepton Decays to e{sup -{nu}}{sub e{nu}{tau}}, {mu}{sup -{nu}}{sub {mu}{nu}{tau}}, {pi}{sup -{nu}}{sub {tau},} and K{sup -{nu}}{sub {tau}}

    SciTech Connect

    Aubert, B.; Karyotakis, Y.; Lees, J. P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D. N.; Kerth, L. T.; Kolomensky, Yu. G.; Lynch, G.

    2010-07-30

    Using 467 fb{sup -1} of e{sup +}e{sup -} annihilation data collected with the BABAR detector, we measure (B({tau}{sup -{yields}}{mu}-{nu}{sub {mu}{nu}{tau}}))/B({tau}{sup -{yields}}e{sup -{nu}}{sub e{nu}{tau}})=(0.9796{+-}0.0016{+-}0.0036), (B({tau}{sup -{yields}}{pi}-{nu}{sub {tau}})/B({tau}{sup -{yields}}e{sup -{nu}}{sub e{nu}{tau}}))=(0.5945{+-}0.0014{+-}0.0061), and (B({tau}{sup -{yields}}K{sup -{nu}}{sub {tau}})/B({tau}{sup -{yields}}e{sup -{nu}}{sub e{nu}{tau}}))=(0.03882{+-}0.00032{+-}0.00057), where the uncertainties are statistical and systematic, respectively. From these precision {tau} measurements, we test the standard model assumption of {mu}-e and {tau}-{mu} charge current lepton universality and provide determinations of |V{sub us}| experimentally independent of the decay of a kaon.

  14. Kaon content of three-prong decays of the tau lepton

    SciTech Connect

    Eastman, J.J.

    1990-12-01

    We present a series of measurements involving the production of charged kaons in three-prong hadronic decays of the {tau} lepton. The data sample was obtained with the TPC/Two-Gamma detector facility at PEP. We set a limit on the branching fraction BR({tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sup {minus}}K{sup 0}) < 0.26% at the 95% confidence level. The process {tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sup {minus}}K{sup 0} is related via SU(3) to the second-class current decay {tau}{sup {minus}} {yields} {nu}{sub {tau}}{pi}{sup {minus}}{eta}. We also present new measurements of the three-prong branching fractions BR({tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sup {minus}}{pi}{sup +}{pi}{sup {minus}} + neutrals) = 0.70 (+0.20/{minus}0.17)% and BR({tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sup {minus}}K{sup +}{pi}{sup {minus}} + neutrals) = 0.16 (+0.10/{minus}0.07)%. 68 refs., 29 figs., 15 tabs.

  15. Search for Rare Multi-Pion Decays of the Tau Lepton Using the BABAR Detector

    SciTech Connect

    Ter-Antonyan, Ruben

    2007-09-18

    A search for the decay of the {tau} lepton to rare multi-pion final states is performed using the BABAR detector at the PEP-II asymmetric-energy e+e- collider. The analysis uses 232 fb-1 of data at center-of-mass energies on or near the {Upsilon}(4S) resonance. In the search for the {tau}- {yields} 3{pi}-2{pi}+2{pi}{sup 0}{nu}{sub {tau}} decay, we observe 10 events with an expected background of 6.5{sup +2.0}{sub -1.4} events. In the absence of a signal, we calculate the decay branching ratio upper limit {beta}({tau}- {yields} 3{pi}-2{pi}+2{pi}{sup 0}{nu}{sub {tau}}) < 3.4 x 10{sup -6} at the 90% confidence level. This is more than a factor of 30 improvement over the previously established limit. In addition, we search for the exclusive decay mode {tau}- {yields} 2{omega}{pi}-{nu}{sub {tau}} with the further decay of {omega} {yields} {pi}-{pi}+{pi}{sup 0}. We observe 1 event, expecting 0.4{sup +1.0}{sub -0.4} background events, and calculate the upper limit {beta}{tau}-{yields} 2{omega}{pi}-{nu}{sub {tau}} < 5.4 x 10{sup -7} at the 90% confidence level. This is the first upper limit for this mode.

  16. Search for doubly charged Higgs bosons with lepton-flavour-violating decays involving tau leptons

    SciTech Connect

    Aaltonen, T.

    2007-12-01

    The authors search for pair production of doubly charged Higgs particles (H{sup {+-}{+-}}) followed by decays into electron-tau (e{tau}) and muon-tau ({mu}{tau}) pairs using a data set corresponding to an integrated luminosity of 350 pb{sup -1} collected from {bar p}p collisions at {radical}s = 1.96 TeV by the CDF II experiment. They search separately for cases where three or four final-state leptons are detected, and then combine the results into limits for each exclusive flavor decay mode of the H{sup {+-}{+-}}. Assuming 100% branching ratios of the H{sup {+-}{+-}} to left-handed e{tau} ({mu}{tau}) pairs, they set an H{sup {+-}{+-}} lower mass limit of 114 (112) GeV/c{sup 2} at the 95% confidence level (C.L.).

  17. Search for Lepton Flavor Violation in the Decay tau -> electron gamma

    SciTech Connect

    Aubert, B.; Barate, R.; Boutigny, D.; Couderc, F.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Tisserand, V.; Zghiche, A.; Grauges, E.; Palano, A.; Pappagallo, M.; Pompili, A.; Chen, J.C.; Qi, N.D.; Rong, G.; Wang, P.; Zhu, Y.S.; Eigen, G.; Ofte, I.; Stugu, B. /Bergen U. /LBL, Berkeley /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /Bristol U. /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /Ferrara U. /INFN, Ferrara /Frascati /Genoa U. /INFN, Genoa /Harvard U. /Heidelberg U. /Karlsruhe U., EKP /Imperial Coll., London /Iowa U. /Iowa State U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT, LNS /McGill U. /Milan U. /INFN, Milan /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /Naples U. /INFN, Naples /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /Padua U. /INFN, Padua /Paris U., VI-VII /Pennsylvania U. /Perugia U. /INFN, Perugia /Pisa U. /INFN, Pisa /Prairie View A-M /Princeton U. /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /South Carolina U. /SLAC /Stanford U., Phys. Dept. /SUNY, Stony Brook /Tennessee U. /Texas U. /Texas U., Dallas /Turin U. /INFN, Turin /Trieste U. /INFN, Trieste /Valencia U., IFIC /Vanderbilt U. /Victoria U. /Warwick U. /Wisconsin U., Madison /Yale U. /Basilicata U., Potenza

    2005-08-26

    A search for the non-conservation of lepton flavor in the decay {tau}{sup {+-}} {yields} e{sup {+-}}{gamma} has been performed with 2.07 x 10{sup 8} e{sup +}e{sup -} {yields} {tau}{sup +}{tau}{sup -} events collected by the BABAR detector at the PEP-II storage ring at a center-of-mass energy near 10.58 GeV. They find no evidence for a signal and set an upper limit on the branching ratio of {Beta}({tau}{sup {+-}} {yields} e{sup {+-}}{gamma}) < 1.1 x 10{sup -7} at 90% confidence level.

  18. Search for lepton flavor violation in the decay tau+/--->e+/-gamma.

    PubMed

    Aubert, B; Barate, R; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Pappagallo, M; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Chevalier, N; Cottingham, W N; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, A E; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Mommsen, R K; Roethel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Weinstein, A J R; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; del Re, D; Hadavand, H K; Hill, E J; Macfarlane, D B; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Minamora, J S; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nauenberg, U; Olivas, A; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Zeng, Q; Altenburg, D; Feltresi, E; Hauke, A; Spaan, B; Brandt, T; Brose, J; Dickopp, M; Klose, V; Lacker, H M; Nogowski, R; Otto, S; Petzold, A; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Bernard, D; Bonneaud, G R; Grenier, P; Schrenk, S; Thiebaux, Ch; Vasileiadis, G; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Xie, Y; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Piemontese, L; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Patteri, P; Peruzzi, I M; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Won, E; Wu, J; Dubitzky, R S; Langenegger, U; Marks, J; Schenk, S; Uwer, U; Schott, G; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Nash, J A; Nikolich, M B; Vazquez, W Panduro; Chai, X; Charles, M J; Mader, W F; Mallik, U; Mohapatra, A K; Ziegler, V; Cochran, J; Crawley, H B; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Yi, J; Arnaud, N; Davier, M; Giroux, X; Grosdidier, G; Höcker, A; Le Diberder, F; Lepeltier, V; Lutz, A M; Oyanguren, A; Petersen, T C; Plaszczynski, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Parry, R J; Payne, D J; Schofield, K C; Touramanis, C; Cormack, C M; Di Lodovico, F; Menges, W; Sacco, R; Brown, C L; Cowan, G; Flaecher, H U; Green, M G; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Edgar, C L; Hodgkinson, M C; Kelly, M P; Lafferty, G D; Naisbit, M T; Williams, J C; Chen, C; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Kofler, R; Koptchev, V B; Li, X; Moore, T B; Saremi, S; Staengle, H; Willocq, S; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Taras, P; Viaud, B; Nicholson, H; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M; Bulten, H; Raven, G; Snoek, H L; Wilden, L; Jessop, C P; Losecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonyan, R; Wong, Q K; Brau, J; Frey, R; Igonkina, O; Lu, M; Potter, C T; Sinev, N B; Strom, D; Strube, J; Torrence, E; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; Del Buono, L; de la Vaissière, Ch; Hamon, O; John, M J J; Leruste, Ph; Malclès, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Biasini, M; Covarelli, R; Pacetti, S; Pioppi, M; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Morganti, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Safai Tehrani, F; Voena, C; Schröder, H; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Gopal, G P; Olaiya, E O; Wilson, F F; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Graziani, G; Hamel de Monchenault, G; Kozanecki, W; Legendre, M; London, G W; Mayer, B; Vasseur, G; Yèche, Ch; Zito, M; Purohit, M V; Weidemann, A W; Wilson, J R; Yumiceva, F X; Abe, T; Allen, M T; Aston, D; Bartoldus, R; Berger, N; Boyarski, A M; Buchmueller, O L; Claus, R; Coleman, J P; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W; Fan, S; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Luth, V; Lynch, H L; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; van Bakel, N; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Ahmed, M; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bona, M; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Martinez-Vidal, F; Panvini, R S; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Graham, M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihalyi, A; Pan, Y; Pierini, M; Prepost, R; Tan, P; Wu, S L; Yu, Z; Neal, H

    2006-02-01

    A search for the nonconservation of lepton flavor in the decay tau+/--->e+/-gamma has been performed with 2.07x10(8) e+e--->tau+tau- events collected by the BABAR detector at the SLAC PEP II storage ring at a center-of-mass energy near 10.58 GeV. We find no evidence for a signal and set an upper limit on the branching ratio of Beta(tau+/--->e+/-gamma)<1.1x10(-7) at 90% confidence level. PMID:16486807

  19. Studies of the Strange Hadronic Tau Decay Tau- to K0(S) Pi- Nu-Tau Using the BaBar Detector

    SciTech Connect

    Lyon, Andrew J.; /Manchester U. /SLAC

    2006-01-27

    A study of the decay {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -} {nu}{sub {tau}} (K{sub S}{sup 0} {yields} {pi}{sup +}{pi}{sup -}) using the BABAR detector is presented. Using 124.4 fb{sup -1} of data we measure {Beta}({tau}{sup -} {yields} {bar K}{sup 0}{pi}{sup -}{nu}{sub {tau}}) = (0.830 {+-} 0.005(stat) {+-} 0.042(syst))%, which is the world's most precise measurement to date of this branching ratio, and is consistent with the current world average. This preliminary result, unlike most of the {Beta}({tau}{sup -} {yields} {bar K}{sup 0}{pi}{sup -}{nu}{sub {tau}}) measurements already published, is systematics dominated and so the biggest future improvement to this number should come from reducing the systematic uncertainties in the analysis. A study of the K{pi} mass spectrum, from which the strange (K{pi}) spectral function can be measured, reveals excess contributions above the K*(892) tail at higher K{pi} mass. While in the past this has been thought to be due to K*(892) - K*(1410) interference, we find that the K*(1410), whose branching ratio to K{pi} is approximately 7%, seems insufficient to explain the excess mass observed in the data. Instead, we perform a fit using a K*(892) - K*(1680) interference model and find better agreement. The discrepancy that remains could be due to an s-wave contribution to the interference that is not parameterized in the model used, and/or detector smearing that is not accounted for in our fit. We also attempt to find an s-wave contribution to the K{pi} mass spectrum by searching for an sp-interference effect. While we find a hint that such an effect exists, we have neither the confidence in the statistics nor systematics in the higher K{pi} mass region to announce an observation. We conclude that it would be a worthwhile study to pursue.

  20. Developmental regulation of tau phosphorylation, tau kinases, and tau phosphatases

    PubMed Central

    Yu, Yang; Run, Xiaoqin; Liang, Zhihou; Li, Yi; Liu, Fei; Liu, Ying; Iqbal, Khalid; Grundke-Iqbal, Inge; Gong, Cheng-Xin

    2009-01-01

    Tau is a neuronal microtubule-associated protein. Its hyperphosphorylation plays a critical role in Alzheimer disease (AD). Expression and phosphorylation of tau are regulated developmentally, but its dynamic regulation and the responsible kinases or phosphatases remain elusive. Here, we studied the developmental regulation of tau in rats during development from embryonic day 15 through the age of 24 months. We found that tau expression increased sharply during the embryonic stage and then became relatively stable, whereas tau phosphorylation was much higher in developing brain than in mature brain. However, the extent of tau phosphorylation at seven of the 14 sites studied was much less in developing brain than in AD brain. Tau phosphorylation during development matched the period of active neurite outgrowth in general. Tau phosphorylation at various sites had different topographic distributions. Several tau kinases appeared to regulate tau phosphorylation collectively at overlapping sites, and the decrease of overall tau phosphorylation in adult brain might be due to the higher levels of tau phosphatases in mature brain. These studies provide new insight into the developmental regulation of site-specific tau phosphorylation and identify the likely sites required for the abnormal hyperphosphorylation of tau in AD. PMID:19183272

  1. Effects of W/sub R/ and charged Higgs in the leptonic decay of /tau/

    SciTech Connect

    Tsai, Yung Su

    1989-07-01

    Experimental test of the existence of the right-hand W boson and the charged Higgs particle is suggested. The experiment involves measurement of muon polarization from the decay of polarized /tau/'s. 8 refs., 2 figs., 1 tab.

  2. Theory of Higgs to tau tau signatures at the LHC

    NASA Astrophysics Data System (ADS)

    Yokoya, Hiroshi

    2014-08-01

    In this report, selected topics of tau leptons are collected in view of the high-energy collider experiments and the Higgs-boson search. Those topics include decay modes, tau-jet tagging, collinear approximation and the tau polarization. Using these unique properties of tau leptons, it is possible to observe various properties of the Higgs boson or the associated scalars in the extended Higgs models at the LHC.

  3. Search for anomalous couplings in the decay of polarized Z bosons to tau lepton pairs

    SciTech Connect

    Torrence, E.C.

    1997-06-01

    Using a sample of 4,500 polarized Z decays to {tau} lepton pairs accumulated with the SLD detector at the SLAC Linear Collider (SLC) in 1993-95, a search has been made for anomalous couplings in the neutral current reaction e{sup +}e{sup {minus}}{yields}{tau}{sup +}{tau}{sup {minus}}. A measurement of the CP violating Weak Electric Dipole Moment (WEDM) and the CP conserving Weak Magnetic Dipole Moment (WMDM) of the {tau} lepton has been performed by considering the transverse spin polarization of {tau} leptons produced at the Z pole. Using a maximum likelihood technique, the observed {tau} decay spectra in the e, {mu}, {pi}, and {rho} decay channels are used to infer the net transverse polarization of the underlying tau leptons, and a fit for the anomalous dipole moments is performed. No evidence for these dipole movements is observed, and limits are placed on both the real and imaginary parts of the WEDM and WMDM.

  4. Search for the Decay $\\tau^- \\rightarrow 3\\pi^- 2\\pi^+2\\pi^0 \

    SciTech Connect

    Aubert, B.

    2006-04-10

    A search for the decay of the {tau} lepton to five charged and two neutral pions is performed using data collected by the BABAR detector at the PEP-II asymmetric-energy e{sup +}e{sup -} collider. The analysis uses 232 fb{sup -1} of data at center-of-mass energies on or near the {Upsilon}(4S) resonance. We observe 10 events with an expected background of 6.5{sub -1.4}{sup +2.0} events. In the absence of a signal, we set the limit on the branching ratio {Beta}({tau}{sup -} {yields} 3{pi}{sup -}2{pi}{sup +}2{pi}{sup 0}{nu}{sub {tau}}) < 3.4 x 10{sup -6} at the 90% confidence level. This is a significant improvement over the previously established limit. In addition, we search for the decay mode {tau}{sup -} {yields} 2{omega}{pi}{sup -}{nu}{sub {tau}}. We observe 1 event with an expected background of 0.4{sub -0.4}{sup +1.0} events and calculate the upper limit {Beta}({tau}{sup -} {yields} 2{omega}{pi}{sup -}{nu}{sub {tau}}) < 5.4 x 10{sup -7} at the 90% confidence level. This is the first upper limit for this mode.

  5. A Search for the Decay Modes B +/- to h +/- tau l

    SciTech Connect

    Lees, J.P.

    2012-07-20

    We present a search for the lepton flavor violating decay modes B{sup {+-}} {yields} h{sup {+-}} {tau}{ell} (h = K, {pi}; {ell} = e, {mu}) using the BABAR data sample, which corresponds to 472 million B{bar B} pairs. The search uses events where one B meson is fully reconstructed in one of several hadronic final states. Using the momenta of the reconstructed B, h, and {ell} candidates, we are able to fully determine the {tau} four-momentum. The resulting {tau} candidate mass is our main discriminant against combinatorial background. We see no evidence for B{sup {+-}} {yields} h{sup {+-}} {tau}{ell} decays and set a 90% confidence level upper limit on each branching fraction at the level of a few times 10{sup -5}.

  6. Lepton flavor violating {tau} decays in the type-III seesaw mechanism

    SciTech Connect

    Arhrib, Abdesslam; Benbrik, Rachid; Chen, C.-H.

    2010-06-01

    In this paper, the lepton flavor violating {tau}{yields}lP(V) (P, V={pi}{sup 0}, {eta}, {eta}{sup '}, {rho}{sup 0}, {omega}, {phi}) and {tau}{yields}3l (l=e, {mu}) decays are studied in the framework of the type-III seesaw model, in which new triplet fermions with a zero hypercharge (Y=0) interact with ordinary lepton doublets via Yukawa couplings, and affect tree-level leptonic Z-boson couplings. We investigate the experimental bound from the leptonic Z decay to get constraints on the existing parameters space. We predict that the upper limits on the branching ratios of {tau}{yields}lP(V) and {tau}{yields}3l can reach the experimental current limits.

  7. Evidence for the 125 GeV Higgs boson decaying to a pair of $\\tau$ leptons

    SciTech Connect

    Chatrchyan, Serguei

    2014-01-20

    A search for a standard model Higgs boson decaying into a pair of tau leptons is performed using events recorded by the CMS experiment at the LHC in 2011 and 2012. The dataset corresponds to an integrated luminosity of 4.9 inverse femtobarns at a centre-of-mass energy of 7 TeV and 19.7 inverse femtobarns at 8 TeV. Each tau lepton decays hadronically or leptonically to an electron or a muon, leading to six different final states for the tau-lepton pair, all considered in this analysis. An excess of events is observed over the expected background contributions, with a local significance larger than 3 standard deviations for m[H] values between 115 and 130 GeV. The best fit of the observed H to tau tau signal cross section for m[H] = 125 GeV is 0.78 +- 0.27 times the standard model expectation. These observations constitute evidence for the 125 GeV Higgs boson decaying to a pair of tau leptons.

  8. Evidence for the 125 GeV Higgs boson decaying to a pair of $$\\tau$$ leptons

    DOE PAGESBeta

    Chatrchyan, Serguei

    2014-01-20

    A search for a standard model Higgs boson decaying into a pair of tau leptons is performed using events recorded by the CMS experiment at the LHC in 2011 and 2012. The dataset corresponds to an integrated luminosity of 4.9 inverse femtobarns at a centre-of-mass energy of 7 TeV and 19.7 inverse femtobarns at 8 TeV. Each tau lepton decays hadronically or leptonically to an electron or a muon, leading to six different final states for the tau-lepton pair, all considered in this analysis. An excess of events is observed over the expected background contributions, with a local significance largermore » than 3 standard deviations for m[H] values between 115 and 130 GeV. The best fit of the observed H to tau tau signal cross section for m[H] = 125 GeV is 0.78 +- 0.27 times the standard model expectation. These observations constitute evidence for the 125 GeV Higgs boson decaying to a pair of tau leptons.« less

  9. Search for Lepton Flavour Violating Decays Tau -> l Ks with the BABAR Detector

    SciTech Connect

    Cenci, Riccardo; /SLAC

    2009-03-20

    We present the search for the lepton flavour violating decay {tau} {yields} lK{sup 0}{sub s} with the BaBar experiment data. This process and many other lepton flavour violating {tau} decays, like {tau} {yields} {mu}{gamma} and {tau} {yields} lll, are one of the most promising channel to search for evidence of new physics. According to the Standard Model and the neutrino mixing parameters, branching fractions are estimated well below 10{sup -14}, but many models of new physics allow for branching fractions values close to the present experimental sensitivity. This analysis is based on a data sample of 469fb{sup -1} collected by BABAR detector at the PEP-II storage ring from 1999 to 2007, equivalent to 431 millions of {tau} pairs. the BABAR experiment, initially designed for studying CP violation in B mesons, has demonstrated to be one of the most suitable environments for studying {tau} decays. The tracking system, the calorimeter and the particle identification of BABAR, together with the knowledge of the {tau} initial energy, allow an extremely powerful rejection of background events that, for this analysis, is better than 10{sup -9}. Being {tau} {yields} lK{sup 0}{sub s} a decay mode without neutrinos, the signal {tau} decay can be fully reconstructed. Kinematical constraints are used in a fit that provides a decay tree reconstruction with a high resolution. For this analysis MC simulated events play a decisive role for estimating the signal efficiency and study the residual background. High statistics MC sample are produced simulating detector conditions for different periods of data collection, in order to reduce any discrepancies with the data. When discrepancies can not be removed, we perform studies to compute a correction factor or an estimation of systematic errors that need to be included in the final measurement. A significant improvement of the current result can be reached only with a higher statistics and, therefore, with a new collider providing a luminosity from 10 to 100 times more than PEP-II. A new detector, with improved performance and able to collect data in a high background environment, is also requested to fully exploit the capability of such amount of data. In fact, only keeping the efficiency and the background as similar as possible to present ones, we will be able to scale almost linearly the estimated upper limit according to the luminosity. The strong potential of improvement for the search of lepton flavour violation {tau} decays makes the building of such a machine highly desirable.

  10. Observation of the Semileptonic Decays B to D*taunu and Evidence for B to D tau nu

    SciTech Connect

    B., Aubert

    2007-09-14

    We present measurements of the semileptonic decays B{sup -} {yields} D{sup 0}{tau}{sup -}{bar {nu}}{sub {tau}}, B{sup -} {yields} D{sup *0}{tau}{sup -}{bar {nu}}{sub {tau}}, B{sup -} {yields} D{sup +}{tau}{sup -}{bar {nu}}{sub {tau}}, and B{sup -} {yields} D{sup *+}{tau}{sup -}{bar {nu}}{sub {tau}}, which are potentially sensitive to non-Standard Model amplitudes, The data sample comprises 232 x 10{sup 6} {Upsilon}(4s) {yields} B{bar B} decays collected with the BABAR detector. From a combined fit to B{sup -} and {bar B}{sup 0} channels, we obtain the branching fractions {beta}(B {yields} D{sub {tau}}{sup -}{bar {nu}}{sub {tau}}) = (0:86 {+-} 0:24 {+-} 0:11 {+-} 0:06)% and {beta}(B {yields} D*{tau}{sup -}{bar {nu}}{sub {tau}}) = (1:62 {+-} 0:31 {+-} 0:10 {+-} 0:05)% (normalized for the {bar B}{sup 0}), , where the uncertainties are statistical, systematic, and normalization-mode-related.

  11. Heavy scalar tau decays in the complex MSSM: a full one-loop analysis

    NASA Astrophysics Data System (ADS)

    Heinemeyer, S.; Schappacher, C.

    2012-09-01

    We evaluate all two-body decay modes of the heavy scalar tau in the Minimal Supersymmetric Standard Model with complex parameters (cMSSM) and no generation mixing. The evaluation is based on a full one-loop calculation of all decay channels, also including hard and soft QED radiation. The renormalization of the relevant sectors is briefly reviewed. The dependence of the heavy scalar tau decay on the relevant cMSSM parameters is analyzed numerically, including also the decay to Higgs bosons and another scalar lepton or to a tau and the lightest neutralino. We find sizable contributions to many partial decay widths and branching ratios. They are mostly of {O}(5{-}10 %) of the tree-level results, but can go up to 20 %. These contributions are potentially important for the correct interpretation of scalar tau decays at the LHC and, if kinematically allowed, at the ILC or CLIC. The evaluation of the branching ratios of the heavy scalar tau will be implemented into the Fortran code FeynHiggs.

  12. Search for Higgs bosons decaying to tau(+)tau(-) pairs in p(p)over-bar collisions at root s=1.96 TeV

    SciTech Connect

    Abazov, V.M.; Abazov, V. M.; Abbott, B.; Achary, B. S.; Adams, M.; Adams, T.; Alexeev, G. D.; Alkhazov, G.; Alton, A.; Alverson, G.; Alves, G. A.; Aoki, M.; Arov, M.; Askew, A.; Asman, B.; Atramentov, O.; Avila, C.; BackusMayes, J.; Badaud, F.; Bagby, L.; Baldin, B.; Bandurin, D. V.; Banerjee, S.; Barberis, E.; Baringer, P.; Barreto, J.; Bartlett, J. F.; Bassler, U.; Bazterra, V.; Beale, S.; Bean, A.; Begalli, M.; Begel, M.; Belanger-Champagne, C.; Bellantoni, L.; Beri, S. B.; Bernardi, G.; Bernhard, R.; Bertram, I.; Besancon, M.; Beuselinck, R.; Bezzubov, V. A.; Bhat, P. C.; Bhatnagar, V.; Blazey, G.; Blessing, S.; Bloom, K.; Boehnlein, A.; Boline, D.; Boos, E. E.; Borissov, G.; Bose, T.; Brandt, A.; Brandt, O.; Brock, R.; Brooijmans, G.; Bross, A.; Brown, D.; Brown, J.; Bu, X. B.; Buehler, M.; Buescher, V.; Bunichev, V.; Burdin, S.; Burnett, T. H.; Buszello, C. P.; Calpas, B.; Camacho-Perez, E.; Carrasco-Lizarraga, M. A.; Casey, B. C. K.; Castilla-Valdez, H.; Chakrabarti, S.; Chakraborty, D.; Chan, K. M.; Chandra, A.; Chen, G.; Chevalier-Thery, S.; Cho, D. K.; Cho, S. W.; Choi, S.; Choudhary, B.; Cihangir, S.; Claes, D.; Clutter, J.; Cooke, M.; Cooper, W. E.; Corcoran, M.; Couderc, F.; Cousinou, M. -C.; Croc, A.; Cutts, D.; Das, A.; Davies, G.; De, K.; de Jong, S. J.; De La Cruz-Burelo, E.; Deliot, F.; Demarteau, M.; Demina, R.; Denisov, D.; Denisov, S. P.; Desai, S.; Deterre, C.; DeVaughan, K.; Diehl, H. T.; Diesburg, M.; Ding, P. F.; Dominguez, A.; Dorland, T.; Dubey, A.; Dudko, L. V.; Duggan, D.; Duperrin, A.; Dutt, S.; Dyshkant, A.; Eads, M.; Edmunds, D.; Ellison, J.; Elvira, V. D.; Enari, Y.; Evans, H.; Evdokimov, A.; Evdokimov, V. N.; Facini, G.; Ferbel, T.; Fiedler, F.; Filthaut, F.; Fisher, W.; Fisk, H. E.; Fortner, M.; Fox, H.; Fuess, S.; Garcia-Bellido, A.; Gavrilov, V.; Gay, P.; Geng, W.; Gerbaudo, D.; Gerber, C. E.; Gershtein, Y.; Ginther, G.; Golovanov, G.; Goussiou, A.; Grannis, P. D.; Greder, S.; Greenlee, H.; Greenwood, Z. D.; Gregores, E. M.; Grenier, G.; Gris, Ph.; Grivaz, J. -F.; Grohsjea, A.; Gruenendahl, S.; Gruenewald, M. W.; Guillemin, T.; Guo, F.; Gutierrez, G.; Gutierrez, P.; Haas, A.; Hagopia, S.; Haley, J.; Hang, L.; Harder, K.; Harein, A.; Hauptman, J. M.; Hays, J.; Head, T.; Hebbeker, T.; Hedin, D.; Hegab, H.; Heinson, A. P.; Heintz, U.; Hensel, C.; Heredia-De La Cruz, I.; Herner, K.; Hesketh, G.; Hildreth, M. D.; Hirosky, R.; Hoangau, T.; Hobbs, J. D.; Hoeneisen, B.; Hohlfeld, M.; Hubacek, Z.; Huske, N.; Hynek, V.; Lashvili, I.; Ilchenko, Y.; Illingworth, R.; Ito, A. S.; Jabeen, S.; Jaffre, M.; Jamin, D.; Jayasinghe, A.; Jesik, R.; Johns, K.; Johnson, M.; Johnston, D.; Jonckheere, A.; Jonsson, P.; Joshi, J.; Jung, A. W.; Juste, A.; Kaadze, K.; Kajfasz, E.; Karmanov, D.; Kasper, P. A.; Katsanos, I. I.; Kehoe, R.; Kermiche, S.; Khalatyan, N.; Khanov, A.; Kharchilava, A.; Kharzheev, Y. N.; Kirby, M. H.; Kohli, J. M.; Kozelov, A. V.; Kraus, J.; Kulikov, S.; Kumar, A.; Kupco, A.; Kurca, T.; Kuzmin, V. A.; Kvita, J.; Lammers, S.; Landsberg, G.; Lebrun, P.; Lee, H. S.; Lee, S. W.; Lee, W. M.; Lellouch, J.; Li, L.; Li, Q. Z.; Lietti, S. M.; Lim, J. K.; Lincoln, D.; Linnemann, J.; Lipaev, V. V.; Lipton, R.; Liu, Y.; Liu, Z.; Lobodenko, A.; Lokajicek, M.; de Sa, R. Lopes; Lubatti, H. J.; Luna-Garcia, R.; Lyon, A. L.; Maciel, A. K. A.; Mackin, D.; Madar, R.; Magana-Villalba, R.; Malik, S.; Malyshev, V. L.; Maravin, Y.; Martinez-Ortega, J.; McCarthy, R.; McGivern, C. L.; Meijer, M. M.; Melnitchouk, A.; Menezes, D.; Mercadante, P. G.; Merkin, M.; Meyer, A.; Meyer, J.; et al.

    2012-02-01

    We present a search for the production of neutral Higgs bosons decaying into {tau}{sup +}{tau}{sup -} pairs in p{bar p} collisions at a center-of-mass energy of 1.96 TeV. The data, corresponding to an integrated luminosity of 5.4 fb{sup -1}, were collected by the D0 experiment at the Fermilab Tevatron Collider. We set upper limits at the 95% C.L. on the product of production cross section and branching ratio for a scalar resonance decaying into {tau}{sup +}{tau}{sup -} pairs, and we interpret these limits as limits on the production of Higgs bosons in the minimal supersymmetric standard model (MSSM) and as constraints in the MSSM parameter space.

  13. Search for Higgs bosons decaying into tau pairs in ppbar collisions at D0

    SciTech Connect

    Owen, Mark A.; /Manchester U.

    2008-08-01

    A search for neutral Higgs bosons decaying into tau pairs is presented using data in p{bar p} collisions at {radical}s = 1.96 TeV. One of the tau leptons is identified via its decay into an electron or muon and the other via its decay into a hadronic final state. The data, corresponding to an integrated luminosity of around 1.0 fb{sup -1}, were collected with the D0 detector at the Fermilab Tevatron collider between April 2002 and February 2006. No significant excess of events above the background expectation is observed and limits on the cross section times branching ratio for neutral Higgs bosons decaying into tau pairs, p{bar p} {yields} {phi} {yields} {tau}{sup +}{tau}{sup -}, are set. The cross section limits are interpreted as exclusions in the parameter space of the minimal supersymmetric Standard Model, resulting in exclusions in the range 40 < tan{beta} < 70 for M{sub A} < 200 GeV. Finally, the effect of Higgs bosons with a large total width is considered and the first model independent correction to the cross section limits for the width effect is presented.

  14. The form factors for hadronic tau decay using background field method

    NASA Astrophysics Data System (ADS)

    Kimura, Daiji; Lee, Kang Young; Morozumi, Takuya

    2014-08-01

    In the two body hadronic tau decays, such as ? ? K? (?) ?, vector mesons play important role. Belle and Babar measured hadronic invariant mass spectrum of ? ? K?? decay. To compare the spectrum with theoretical prediction, we develop the chiral Lagrangian with vector mesons in [D. Kimura, K. Y. Lee and T. Morozumi, arxiv:arXiv:1201.1794 [hep-ph

  15. Surprising theoretical results on the decay rate of the /tau/ lepton

    SciTech Connect

    Braaten, E.

    1988-10-24

    Corrections to the naive prediction for the inclusive semihadronic decay rate of the /tau/ lepton contain several surprises: electroweak corrections are significant, nonperturbative QCD corrections can be treated systematically, and the order ed /sub s/T perturbative QCD corrections are enormous. The possibility of precise theoretical predictions of the decay rate is discussed. 10 refs.

  16. What Renders TAU Toxic

    PubMed Central

    Gtz, Jrgen; Xia, Di; Leinenga, Gerhard; Chew, Yee Lian; Nicholas, Hannah R.

    2013-01-01

    TAU is a microtubule-associated protein that under pathological conditions such as Alzheimers disease (AD) forms insoluble, filamentous aggregates. When 20?years after TAUs discovery the first TAU transgenic mouse models were established, one declared goal that was achieved was the modeling of authentic TAU aggregate formation in the form of neurofibrillary tangles. However, as we review here, it has become increasingly clear that TAU causes damage much before these filamentous aggregates develop. In fact, because TAU is a scaffolding protein, increased levels and an altered subcellular localization (due to an increased insolubility and impaired clearance) result in the interaction of TAU with cellular proteins with which it would otherwise either not interact or do so to a lesser degree, thereby impairing their physiological functions. We specifically discuss the non-axonal localization of TAU, the role phosphorylation has in TAU toxicity and how TAU impairs mitochondrial functions. A major emphasis is on what we have learned from the four available TAU knock-out models in mice, and the knock-out of the TAU/MAP2 homolog PTL-1 in worms. It has been proposed that in human pathological conditions such as AD, a rare toxic TAU species exists which needs to be specifically removed to abrogate TAUs toxicity and restore neuronal functions. However, what is toxic in one context may not be in another, and simply reducing, but not fully abolishing TAU levels may be sufficient to abrogate TAU toxicity. PMID:23772223

  17. Tau identification at the Tevatron

    SciTech Connect

    Levy, Stephen; /Chicago U., EFI

    2005-07-01

    Methods for reconstructing and identifying the hadronic decays of tau leptons with the CDF and D0 detectors at the Fermilab Tevatron collider in Run II are described. Precision electroweak measurements of W and Z gauge boson cross sections are presented as well as results of searches for physics beyond the Standard Model with hadronically decaying tau leptons in the final state.

  18. Identification and energy calibration of hadronically decaying tau leptons with the ATLAS experiment in pp collisions at

    NASA Astrophysics Data System (ADS)

    Aad, G.; Abbott, B.; Abdallah, J.; Abdel Khalek, S.; Abdinov, O.; Aben, R.; Abi, B.; Abolins, M.; AbouZeid, O. S.; Abramowicz, H.; Abreu, H.; Abreu, R.; Abulaiti, Y.; Acharya, B. S.; Adamczyk, L.; Adams, D. L.; Adelman, J.; Adomeit, S.; Adye, T.; Agatonovic-Jovin, T.; Aguilar-Saavedra, J. A.; Agustoni, M.; Ahlen, S. P.; Ahmadov, F.; Aielli, G.; Akerstedt, H.; kesson, T. P. A.; Akimoto, G.; Akimov, A. V.; Alberghi, G. L.; Albert, J.; Albrand, S.; Alconada Verzini, M. J.; Aleksa, M.; Aleksandrov, I. N.; Alexa, C.; Alexander, G.; Alexandre, G.; Alexopoulos, T.; Alhroob, M.; Alimonti, G.; Alio, L.; Alison, J.; Allbrooke, B. M. M.; Allison, L. J.; Allport, P. P.; Aloisio, A.; Alonso, A.; Alonso, F.; Alpigiani, C.; Altheimer, A.; Alvarez Gonzalez, B.; Alviggi, M. G.; Amako, K.; Amaral Coutinho, Y.; Amelung, C.; Amidei, D.; Amor Dos Santos, S. P.; Amorim, A.; Amoroso, S.; Amram, N.; Amundsen, G.; Anastopoulos, C.; Ancu, L. S.; Andari, N.; Andeen, T.; Anders, C. F.; Anders, G.; Anderson, K. J.; Andreazza, A.; Andrei, V.; Anduaga, X. S.; Angelidakis, S.; Angelozzi, I.; Anger, P.; Angerami, A.; Anghinolfi, F.; Anisenkov, A. V.; Anjos, N.; Annovi, A.; Antonaki, A.; Antonelli, M.; Antonov, A.; Antos, J.; Anulli, F.; Aoki, M.; Aperio Bella, L.; Apolle, R.; Arabidze, G.; Aracena, I.; Arai, Y.; Araque, J. P.; Arce, A. T. H.; Arduh, F. A.; Arguin, J.-F.; Argyropoulos, S.; Arik, M.; Armbruster, A. J.; Arnaez, O.; Arnal, V.; Arnold, H.; Arratia, M.; Arslan, O.; Artamonov, A.; Artoni, G.; Asai, S.; Asbah, N.; Ashkenazi, A.; sman, B.; Asquith, L.; Assamagan, K.; Astalos, R.; Atkinson, M.; Atlay, N. B.; Auerbach, B.; Augsten, K.; Aurousseau, M.; Avolio, G.; Axen, B.; Azuelos, G.; Azuma, Y.; Baak, M. A.; Baas, A. E.; Bacci, C.; Bachacou, H.; Bachas, K.; Backes, M.; Backhaus, M.; Backus Mayes, J.; Badescu, E.; Bagiacchi, P.; Bagnaia, P.; Bai, Y.; Bain, T.; Baines, J. T.; Baker, O. K.; Balek, P.; Balli, F.; Banas, E.; Banerjee, Sw.; Bannoura, A. A. E.; Bansil, H. S.; Barak, L.; Baranov, S. P.; Barberio, E. L.; Barberis, D.; Barbero, M.; Barillari, T.; Barisonzi, M.; Barklow, T.; Barlow, N.; Barnes, S. L.; Barnett, B. M.; Barnett, R. M.; Barnovska, Z.; Baroncelli, A.; Barone, G.; Barr, A. J.; Barreiro, F.; Barreiro Guimares da Costa, J.; Bartoldus, R.; Barton, A. E.; Bartos, P.; Bartsch, V.; Bassalat, A.; Basye, A.; Bates, R. L.; Batista, S. J.; Batley, J. R.; Battaglia, M.; Battistin, M.; Bauer, F.; Bawa, H. S.; Beattie, M. D.; Beau, T.; Beauchemin, P. H.; Beccherle, R.; Bechtle, P.; Beck, H. P.; Becker, K.; Becker, S.; Beckingham, M.; Becot, C.; Beddall, A. J.; Bedikian, S.; Beddall, A.; Bednyakov, V. A.; Bee, C. P.; Beemster, L. J.; Beermann, T. A.; Begel, M.; Behr, K.; Belanger-Champagne, C.; Bell, P. J.; Bell, W. H.; Bella, G.; Bellagamba, L.; Bellerive, A.; Bellomo, M.; Belotskiy, K.; Beltramello, O.; Benary, O.; Benchekroun, D.; Bendtz, K.; Benekos, N.; Benhammou, Y.; Benhar Noccioli, E.; Benitez Garcia, J. A.; Benjamin, D. P.; Bensinger, J. R.; Bentvelsen, S.; Berge, D.; Bergeaas Kuutmann, E.; Berger, N.; Berghaus, F.; Beringer, J.; Bernard, C.; Bernat, P.; Bernius, C.; Bernlochner, F. U.; Berry, T.; Berta, P.; Bertella, C.; Bertoli, G.; Bertolucci, F.; Bertsche, C.; Bertsche, D.; Besana, M. I.; Besjes, G. J.; Bessidskaia Bylund, O.; Bessner, M.; Besson, N.; Betancourt, C.; Bethke, S.; Bhimji, W.; Bianchi, R. M.; Bianchini, L.; Bianco, M.; Biebel, O.; Bieniek, S. P.; Bierwagen, K.; Biesiada, J.; Biglietti, M.; Bilbao De Mendizabal, J.; Bilokon, H.; Bindi, M.; Binet, S.; Bingul, A.; Bini, C.; Black, C. W.; Black, J. E.; Black, K. M.; Blackburn, D.; Blair, R. E.; Blanchard, J.-B.; Blazek, T.; Bloch, I.; Blocker, C.; Blum, W.; Blumenschein, U.; Bobbink, G. J.; Bobrovnikov, V. S.; Bocchetta, S. S.; Bocci, A.; Bock, C.; Boddy, C. R.; Boehler, M.; Boek, T. T.; Bogaerts, J. A.; Bogdanchikov, A. G.; Bogouch, A.; Bohm, C.; Boisvert, V.; Bold, T.; Boldea, V.; Boldyrev, A. S.; Bomben, M.; Bona, M.; Boonekamp, M.; Borisov, A.; Borissov, G.; Borri, M.; Borroni, S.; Bortfeldt, J.; Bortolotto, V.; Bos, K.; Boscherini, D.; Bosman, M.; Boterenbrood, H.; Boudreau, J.; Bouffard, J.; Bouhova-Thacker, E. V.; Boumediene, D.; Bourdarios, C.; Bousson, N.; Boutouil, S.; Boveia, A.; Boyd, J.; Boyko, I. R.; Bozic, I.; Bracinik, J.; Brandt, A.; Brandt, G.; Brandt, O.; Bratzler, U.; Brau, B.; Brau, J. E.; Braun, H. M.; Brazzale, S. F.; Brelier, B.; Brendlinger, K.; Brennan, A. J.; Brenner, R.; Bressler, S.; Bristow, K.; Bristow, T. M.; Britton, D.; Brochu, F. M.; Brock, I.; Brock, R.; Bronner, J.; Brooijmans, G.; Brooks, T.; Brooks, W. K.; Brosamer, J.; Brost, E.; Brown, J.; Bruckman de Renstrom, P. A.; Bruncko, D.; Bruneliere, R.; Brunet, S.; Bruni, A.; Bruni, G.; Bruschi, M.; Bryngemark, L.; Buanes, T.; Buat, Q.

    2015-07-01

    This paper describes the trigger and offline reconstruction, identification and energy calibration algorithms for hadronic decays of tau leptons employed for the data collected from pp collisions in 2012 with the ATLAS detector at the LHC center-of-mass energy . The performance of these algorithms is measured in most cases with decays to tau leptons using the full 2012 dataset, corresponding to an integrated luminosity of 20.3 fb. An uncertainty on the offline reconstructed tau energy scale of 2-4 %, depending on transverse energy and pseudorapidity, is achieved using two independent methods. The offline tau identification efficiency is measured with a precision of 2.5 % for hadronically decaying tau leptons with one associated track, and of 4 % for the case of three associated tracks, inclusive in pseudorapidity and for a visible transverse energy greater than 20 . For hadronic tau lepton decays selected by offline algorithms, the tau trigger identification efficiency is measured with a precision of 2-8 %, depending on the transverse energy. The performance of the tau algorithms, both offline and at the trigger level, is found to be stable with respect to the number of concurrent proton-proton interactions and has supported a variety of physics results using hadronically decaying tau leptons at ATLAS.

  19. Analysis of birefringence decay profiles for nucleic acid helices possessing bends: the tau-ratio approach.

    PubMed Central

    Vacano, E; Hagerman, P J

    1997-01-01

    For nucleic acid helices in the 100-200-bp range, a central bend or point of flexibility increases the rate of rotational diffusion. In a transient electric birefringence (TEB) experiment, this increase is manifest as a reduction in the terminal (slowest) birefringence decay time. Previous experimental and theoretical work has demonstrated that the ratio of the decay times for a bent/flexible molecule and its fully duplex (linear) counterpart represents a sensitive, quantifiable measure of the apparent bend angle (tau-ratio approach). In the current work, we have examined the influence of helix parameters (e.g., persistence length, helix rise, diameter) on the tau-ratio for a given bend. The tau-ratio is found to be remarkably insensitive to variations and/or uncertainties in the helix parameters, provided that one employs bent and control molecules with the same sequence and length (apart from the bend itself). Although a single tau-ratio determination normally does not enable one to distinguish between fixed and flexible bends, such a distinction can be made from a set of tau-ratios for molecules possessing two variably phased bends. A number of additional uncertainties are examined, including errors in the estimation of the dimensions of nonhelix elements that are responsible for bends; such errors can, in principle, be estimated by performing a series of measurements for molecules of varying length. Images FIGURE 1 PMID:9199795

  20. A Search for the Rare Leptonic B- to tau- anti-neutrino Recoiling against B+ to Decays to anti-D*0 l+ Lepton-neutrino

    SciTech Connect

    Datta, Mousumi; /Wisconsin U., Madison

    2006-10-17

    This thesis describes a search for the decay B{sup -} {yields} {tau}{sup -}{bar {nu}}{sub {tau}} in 231.8 x 10{sup 6} {Upsilon}(4S) decays recorded with the BABAR detector at the SLAC PEP-II B-Factory. A sample of events with one reconstructed exclusive semi-leptonic B decay (B{sup +} {yields} {bar D}*{sup 0} {ell}{sup +}{nu}{sub {ell}}) is selected, and in the recoil a search for B{sup -} {yields} {tau}{sup -} {bar {nu}}{sub {tau}} signal is performed in the following {tau} decay modes: {tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}, {tau}{sup -} {yields} {mu}{sup -}{bar {nu}}{sub {mu}}{nu}{sub {tau}}, {tau}{sup -} {yields} {pi}{sup -}{nu}{sub {tau}}, {tau}{sup -} {yields} {pi}{sup -}{pi}{sup 0}{nu}{sub {tau}}, and {tau}{sup -} {yields} {pi}{sup -}{pi}{sup +}{pi}{sup -}{nu}{sub {tau}}. They find no evidence of signal, and they set a preliminary upper limit on the branching fraction of {beta}(B{sup -} {yields} {tau}{sup -}{bar {nu}}{sub {tau}}) < 2.8 x 10{sup -4} at the 90% confidence level (CL). This result is then combined with a statistically independent BABAR search for B{sup -} {yields} {tau}{sup -}{bar {nu}}{sub {tau}} to give a combined preliminary limit of {Beta}(B{sup -} {yields} {tau}{sup -}{bar {nu}}{sub {tau}}) < 2.6 x 10{sup -4} at 90% CL.

  1. Measurement of the Branching Fraction for D8+ rarr tau+nu_tau and Extraction of the Decay Constant f_D_s

    SciTech Connect

    Lees, J.P.; Poireau, V.; Prencipe, E.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D.N.; Hooberman, B.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; Tanabe, T.; Hawkes, C.M.

    2010-06-04

    The branching fraction for the decay D{sub s}{sup +} {yields} {tau}{sup +}{nu}{sub {tau}} with {tau}{sup +} {yields} e{sup +}{bar {nu}}{sub {tau}}, is measured using a data sample corresponding to an integrated luminosity of 427 fb{sup -1} collected at center of mass energies near 10.58 GeV with the BABAR detector at the PEP-II asymmetric-energy e{sup +}e{sup -} collider at SLAC. In the process e{sup +}e{sup -} {yields} c{bar c} {yields} D*{sub s}{sup +} {bar D}{sub TAG}{bar K}X, the D*{sub s}{sup +} meson is reconstructed as a missing particle, and the subsequent decay D*{sub s}{sup +} {yields} D{sub s}{sup +}{gamma} yields an inclusive D{sub s}{sup +} data sample. Here {bar D}{sub TAG} refers to a fully reconstructed hadronic {bar D} decay, {bar K} is a K{sup -} or {bar K}{sup 0}, and X stands for any number of charged or neutral pions. The decay D{sub s}{sup +} {yields} K{sub S}{sup 0}K{sup +} is isolated also, and from ratio of event yields and known branching fractions, {Beta}(D{sub s}{sup +} {yields} {tau}{sup +}{nu}{sub {tau}}) = (4.5 {+-} 0.5 {+-} 0.4 {+-} 0.3)% is determined. The pseudoscalar decay constant is extracted to be f{sub D{sub s}} = (233 {+-} 13 {+-} 10 {+-} 7) MeV, where the first uncertainty is statistical, the second is systematic, and the third results from the uncertainties on the external measurements used as input to the calculation.

  2. Two current experimental problems in heavy lepton physics: tau decay modes and close mass pairs

    SciTech Connect

    Perl, M.L.

    1987-08-01

    This paper investigates tau lepton decay modes and close-mass lepton pairs. The major part of the paper discusses branching functions from experimental and theoretical viewpoints. Finally, the lack of experimental signatures of close-mass lepton pairs are reviewed. 15 refs., 2 figs., 11 tabs. (JDH)

  3. Tau and Tauopathies

    PubMed Central

    Lee, Gloria; Leugers, Chad J.

    2013-01-01

    Tauopathies are age-related neurodegenerative diseases that are characterized by the presence of aggregates of abnormally phosphorylated tau. As tau was originally discovered as a microtubule-associated protein, it has been hypothesized that neurodegeneration results from a loss of the ability of tau to associate with microtubules. However, tau has been found to have other functions aside from the promotion and stabilization of microtubule assembly. It is conceivable that such functions may be affected by the abnormal phosphorylation of tau and might have consequences for neuronal function or viability. This chapter provides an overview of tau structure, functions, and its involvement in neurodegenerative diseases. PMID:22482453

  4. A Search for the Decay B+ ---> Tau+ Nu/Tau at BaBar

    SciTech Connect

    Datta, M.; /Wisconsin U., Madison

    2005-11-02

    Based on an 87-fb{sup -1} dataset collected by the Babar detector at the PEP-II asymmetric-energy B-Factory, a search for D{sup 0}-{bar D}{sup 0} mixing has been made using the semileptonic decay modes D*{sup +} {yields} {pi}{sup +}D{sup 0}, D{sup 0} {yields} Ke{nu} (+c.c.). The use of these modes allows unambiguous flavor tagging and a combined fit of the D{sup 0} decay time and D*{sup +}-D{sup 0} mass difference ({Delta}M) distributions. The high-statistics sample of unmixed semileptonic D{sup 0} decays is used to model the {Delta}M distribution and time-dependence of mixed events directly from the data. Neural networks are used to select events and reconstruct the D{sup 0}. A result consistent with no charm mixing has been obtained, R{sub mix} = 0.0023 {+-} 0.0012 {+-} 0.0004. This corresponds to an upper limit of R{sub mix} < 0.0042 (90% CL).

  5. Search for Lepton Flavour Violating Decays tau- to l- Ks with the BaBar experiment

    SciTech Connect

    Aubert, B.; Bona, M.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Lopez, L.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Abrams, G.S.; Battaglia, M.; Brown, D.N.; Cahn, R.N.; Jacobsen, R.G.; /LBL, Berkeley /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /Bristol U. /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /Frascati /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Karlsruhe U., EKP /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT, LNS /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /INFN, Naples /Naples U. /INFN, Naples /INFN, Naples /Naples U. /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /Pennsylvania U. /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DSM, DAPNIA, Saclay /South Carolina U. /SLAC /Stanford U., Phys. Dept. /SUNY, Albany /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U., IFIC /Victoria U. /Warwick U. /Wisconsin U., Madison

    2009-01-06

    A search for the lepton flavor violating decays {tau}{sup -} {yields} l{sup -} K{sub S}{sup 0} (l = e or {mu}) has been performed using a data sample corresponding to an integrated luminosity of 469 fb{sup -1}, collected with the BABAR detector at the SLAC PEP-II e{sup +}e{sup -} asymmetric energy collider. No statistically significant signal has been observed in either channel and the estimated upper limits on branching fractions are {Beta}({tau}{sup -} {yields} e{sup -} K{sub S}{sup 0}) < 3.3 x 10{sup -8} and {Beta}({tau}{sup -} {yields} {mu}{sup -}K{sub S}{sup 0}) < 4.0 x 10{sup -8} at 90% confidence level.

  6. Search for Lepton Flavour Violation (LFV) in Three-Body Tau Decays at BaBar

    SciTech Connect

    Hodgkinson, M.; /Manchester U.

    2005-08-17

    The results of searches for Lepton Flavour Violating (LFV) decays at the BaBar detector located on the PEP-II collider, using data collected at an e{sup +}e{sup -} energy of 10.58 GeV, are presented. Upper limits at 90% Confidence Level (CL) are established in the range 1-3 x 10{sup -7} for six {tau} {yields} lll modes using 91.5 fb{sup -1} of data and in the range 0.7-4.8 x 10{sup -7} for fourteen {tau} {yields} lhh modes using 221.4 fb{sup -1} of data. The {tau} {yields} lhh results are preliminary.

  7. Search for High-Mass Resonances Decaying into Leptons of Different Flavor (e mu, e tau, mu tau) in p anti-p Collisions at sqrt(s) = 1.96 TeV

    SciTech Connect

    Tu, Yanjun; /Pennsylvania U.

    2008-10-01

    We present a search for high-mass resonances decaying into two leptons of different flavor: e{mu}, e{tau}, and {mu}{tau}. These resonances are predicted by several models beyond the standard model, such as the R-parity-violating MSSM. The search is based on 1 fb{sup -1} of data collected at the Collider Detector at Fermilab (CDF II) in proton anti-proton collisions. Our observations are consistent with the standard model expectations. The results are interpreted to set 95% C.L. upper limits on {sigma} x BR of {tilde {nu}}{sub {tau}} {yields} e{mu}, e{tau}, {mu}{tau}.

  8. The ATLAS Hadronic Tau Trigger

    NASA Astrophysics Data System (ADS)

    Brost, Elizabeth Caitlin

    2014-03-01

    As proton-proton collisions at the LHC reach luminosities close to 1034 cm-2 s-1, the strategies for triggering have become more important than ever for physics analyses. Simplistic single tau lepton triggers suffer from severe rate limitation, despite the sophisticated algorithms used in the tau identification. The development of further fast algorithms and the design of topological selections are the main challenges to allow a large program of physics analysis. The tau triggers provide many opportunities to study new physics beyond the Standard Model, and to get precise measurements of the properties of the Higgs boson decaying to tau-leptons. We present the performance of the hadronic tau trigger taken in Run 1 data with the ATLAS detector at sqrt(s) =8TeV p-p collision. One of the major challenges is to sustain high efficiencies in events with multiple interactions. To do this we introduced faster tracking methods, multivariate selection techniques, and new topological criteria in the software trigger. We present measurements of the trigger efficiency using Z to tau tau events as the application to searches for tau tau resonances, such as the Higgs boson searches. We also outline the upgrade plan expected for Run 2 for the 14(13) TeV LHC pp collisions.

  9. New results on the tau lepton

    SciTech Connect

    Gan, K.K.

    1987-11-01

    This is a review of new results on the tau lepton. The results include precise measurements of the lifetime, measurements of the decay tau/sup -/ ..-->.. ..pi../sup -/2..pi../sup 0/nu/sub tau/ with much improved precision, and limits on decay modes containing eta mesons, including the second-class-current decay tau/sup -/ ..-->.. ..pi../sup -/eta nu/sub tau/. The implications of these new results on the discrepancy in the one-charged-particle decay modes are discussed. 52 refs., 6 figs., 2 tabs.

  10. Observation of the semileptonic decays B-->D*tau-nutau and evidence for B-->Dtau-nutau.

    PubMed

    Aubert, B; Bona, M; Boutigny, D; Karyotakis, Y; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Tico, J Garra; Grauges, E; Lopez, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Pegna, D Lopes; Lynch, G; Mir, L M; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabe, T; Wenzel, W A; Del Amo Sanchez, P; Hawkes, C M; Watson, A T; Koch, H; Schroeder, T; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Gary, J W; Liu, F; Long, O; Shen, B C; Vitug, G M; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Panduro Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, L; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, G; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; Losecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Sekula, S J; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; de la Vaissire, Ch; Hamon, O; Leruste, Ph; Malcls, J; Ocariz, J; Perez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N

    2008-01-18

    We present measurements of the semileptonic decays B--->D0tau-nutau, B--->D*0tau-nutau, B0-->D+tau-nutau, and B0-->D*+tau-nutau, which are potentially sensitive to non-standard model amplitudes. The data sample comprises 232x10(6) Upsilon(4S)-->BB decays collected with the BABAR detector. From a combined fit to B- and B0 channels, we obtain the branching fractions B(B-->Dtau-nutau)=(0.86+/-0.24+/-0.11+/-0.06)% and B(B-->D*tau-nutau)=(1.62+/-0.31+/-0.10+/-0.05)% (normalized for the B0), where the uncertainties are statistical, systematic, and normalization-mode-related. PMID:18232854

  11. Evidence for an excess of B to D(*) Tau Nu decays

    SciTech Connect

    Lees, J.P.; Poireau, V.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Palano, A.; Eigen, G.; Stugu, B.; Brown, David Nathan; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Koch, H.; Schroeder, T.; Asgeirsson, D.J.; Hearty, C.; Mattison, T.S.; McKenna, J.A.; So, R.Y.; Khan, A.; Blinov, V.E.; /more authors..

    2012-10-09

    Based on the full BABAR data sample, we report improved measurements of the ratios R(D{sup (*)}) = {Beta}({bar B} {yields} D{sup (*)} {tau}{sup -}{bar {nu}}{sub {tau}})/{Beta}({bar B} {yields} D{sup (*)} {ell}{sup -}{bar {nu}}{sub {ell}}), where {ell} is either e or {mu}. These ratios are sensitive to new physics contributions in the form of a charged Higgs boson. We measure R(D) = 0.440 {+-} 0.058 {+-} 0.042 and R(D*) = 0.332 {+-} 0.024 {+-} 0.018, which exceed the Standard Model expectations by 2.0{sigma} and 2.7{sigma}, respectively. Taken together, our results disagree with these expectations at the 3.4{sigma} level. This excess cannot be explained by a charged Higgs boson in the type II two-Higgs-doublet model. We also report the observation of the decay {bar B} {yields} D{tau}{sup -} {bar {nu}}{sub {tau}}, with a significance of 6.8{sigma}.

  12. The Tau Lepton and the Search for New Elementary Particle Physics

    SciTech Connect

    Perl, Martin L.

    1998-11-18

    This Fifth International WEIN Symposium is devoted to physics beyond the standard model. This talk is about tau lepton physics, but I begin with the question: do we know how to find new physics in the world of elementary particles? This question is interwoven with the various tau physics topics. These topics are: searching for unexpected tau decay modes; searching for additional tau decay mechanisms; radiative tau decays; tau decay modes of the W, B, and D; decay of the Z{sup 0} to tau pairs; searching for CP violation in tau decay; the tau neutrino, dreams and odd ideas in tau physics; and tau research facilities in the next decades.

  13. Search for CP Violation in $\\tau$ And D Decays With a $K^0_S$ in the Final State

    SciTech Connect

    Martinelli, Maurizio; /Bari U. /INFN, Bari /SLAC

    2012-09-14

    I report the recent searches for CP violation in {tau} and D decays including a K{sub s}{sup 0} in the final state. The analyses herein shown are based on data samples recorded by BABAR and Belle experiments. A brief introduction on CP violation is followed by the summary of the experimental techniques and the results obtained for {tau} and D decays, respectively. Finally, an outlook on future development is provided.

  14. Tau Trigger at the ATLAS Experiment

    SciTech Connect

    Benslama, K.; Kalinowski, A.; Belanger-Champange, C.; Brenner, R.; Bosman, M.; Casado, P.; Osuna, C.; Perez, E.; Vorwerk, V.; Czyczula, Z.; Dam, M.; Xella, S.; Demers, S.; Farrington, S.; Igonkina, O.; Kanaya, N.; Tsuno, S.; Ptacek, E.; Reinsch, A.; Strom, David M.; Torrence, E.; /Oregon U. /Sydney U. /Lancaster U. /Birmingham U.

    2011-11-09

    Many theoretical models, like the Standard Model or SUSY at large tan({beta}), predict Higgs bosons or new particles which decay more abundantly to final states including tau leptons than to other leptons. At the energy scale of the LHC, the identification of tau leptons, in particular in the hadronic decay mode, will be a challenging task due to an overwhelming QCD background which gives rise to jets of particles that can be hard to distinguish from hadronic tau decays. Equipped with excellent tracking and calorimetry, the ATLAS experiment has developed tau identification tools capable of working at the trigger level. This contribution presents tau trigger algorithms which exploit the main features of hadronic tau decays and describes the current tau trigger commissioning activities. Many of the SM processes being investigated at ATLAS, as well as numerous BSM searches, contain tau leptons in their final states. Being able to trigger effectively on the tau leptons in these events will contribute to the success of the ATLAS experiment. The tau trigger algorithms and monitoring infrastructure are ready for the first data, and are being tested with the data collected with cosmic muons. The development of efficiency measurements methods using QCD and Z {yields} {tau}{tau} events is well advanced.

  15. Lifetime measurements and tau physics at PEP

    SciTech Connect

    Gladney, L.D.

    1984-05-01

    Recent updates on the measurements of the tau and D/sup 0/ lifetimes by the Mark II Collaboration and on measurements of the tau and B-hadron lifetimes by the MAC Collaboration are presented. A new determination of an upper limit for the tau neutrino mass by the Mark II Collaboration and a recent measurement of Cabibbo-suppressed tau decay branching ratios from the DELCO Collaboration are also presented. 18 references.

  16. Search For the Lepton-Flavor Violating Decays Y(3S)->e tau and Y(3S)->mu tau

    SciTech Connect

    Aubert, B.

    2008-12-11

    Charged lepton-flavor violating processes are extremely rare in the Standard Model, but they are predicted to occur in several beyond-the-Standard Model theories, including Supersymmetry or models with leptoquarks or compositeness. We present a search for such processes in a sample of 117 x 10{sup 6} {Upsilon}(3S) decays recorded with the BABAR detector. We place upper limits on the branching fractions BF({Upsilon}(3S) {yields} e{sup {+-}}{tau}{sup {-+}}) < 5.0 x 10{sup -6} and BF({Upsilon}(3S) {yields} {mu}{sup {+-}}{tau}{sup {-+}}) < 4.1 x 10{sup -6} at 90% confidence level. These results are used to place lower limits on the mass scale of beyond-the-Standard Model physics contributing to lepton-flavor violating decays of the {Upsilon}(3S).

  17. Measurements of Charged Current Lepton Universality and |Vus| using Tau Lepton Decays to e- v v, __- v v, pi- v and K- v

    SciTech Connect

    Aubert, Bernard; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /INFN, Naples /Naples U. /INFN, Naples /INFN, Naples /Naples U. /NIKHEF, Amsterdam /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /Pennsylvania U. /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2011-06-30

    Using 467 fb{sup -1} of e{sup +}e{sup -} annihilation data collected with the BABAR detector, they measure {Beta}({tau}{sup -} {yields} {mu}{sup -}{bar {nu}}{sub {mu}}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -} {bar {nu}}{sub e}{nu}{sub {tau}}) = (0.9796 {+-} 0.0016 {+-} 0.0036), {Beta}({tau}{sup -} {yields} {pi}{sup -} {nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}) = (0.5945 {+-} 0.0014 {+-} 0.0061), and {Beta}({tau}{sup -} {yields} K{sup -}{nu}{sub {tau}})/{Beta}({tau}{sup -} {yields} e{sup -}{bar {nu}}{sub e}{nu}{sub {tau}}) = (0.03882 {+-} 0.00032 {+-} 0.00057), where the uncertainties are statistical and systematic, respectively. From these precision {tau} measurements, they test the Standard Model assumption of {mu}-e and {tau}-{mu} charge current lepton universality and provide determinations of |V{sub us}| experimentally independent of the decay of a kaon.

  18. Measurement of the {tau} lifetime at SLD

    SciTech Connect

    Abe, K.; Abt, I.; Ahn, C.J.; Akagi, T.; Allen, N.J.; Ash, W.W.; Aston, D.; Baird, K.G.; Baltay, C.; Band, H.R.; Barakat, M.B.; Baranko, G.; Bardon, O.; Barklow, T.; Bazarko, A.O.; Ben-David, R.; Benvenuti, A.C.; Bienz, T.; Bilei, G.M.; Bisello, D.; Blaylock, G.; Bogart, J.R.; Bolton, T.; Bower, G.R.; Brau, J.E.; Breidenbach, M.; Bugg, W.M.; Burke, D.; Burnett, T.H.; Burrows, P.N.; Busza, W.; Calcaterra, A.; Caldwell, D.O.; Calloway, D.; Camanzi, B.; Carpinelli, M.; Cassell, R.; Castaldi, R.; Castro, A.; Cavalli-Sforza, M.; Church, E.; Cohn, H.O.; Coller, J.A.; Cook, V.; Cotton, R.; Cowan, R.F.; Coyne, D.G.; D`Oliveira, A.; Damerell, C.J.S.; Daoudi, M.; De Sangro, R.; De Simone, P.; Dell`Orso, R.; Dima, M.; Du, P.Y.C.; Dubois, R.; Eisenstein, B.I.; Elia, R.; Etzion, E.; Falciai, D.; Fero, M.J.; Frey, R.; Furuno, K.; Gillman, T.; Gladding, G.; Gonzalez, S.; Hallewell, G.D.; Hart, E.L.; Hasegawa, Y.; Hedges, S.; Hertzbach, S.S.; Hildreth, M.D.; Huber, J.; Huffer, M.E.; Hughes, E.W.; Hwang, H.; Iwasaki, Y.; Jackson, D.J.; Jacques, P.; Jaros, J.; Johnson, A.S.; Johnson, J.R.; Johnson, R.A.; Junk, T.; Kajikawa, R.; Kalelkar, M.; Kang, H.J.; Karliner, I.; Kawahara, H.; Kendall, H.W.; Kim, Y.; King, M.E.; King, R.; Kofler, R.R.; Krishna, N.M.; Kroeger, R.S.; Labs, J.F.; Langston, M.; Lath, A.; Lauber, J.A.; Leith, D.W.G.; Liu, M.X.; Liu, X.; Loreti, M.; Lu, A.; Lynch, H.L.; Ma, J.; Mancinelli, G.; Manly, S.; Mantovani, G.; Markiewicz, T.W.; Maruyama, T.; Massetti, R.; Masuda, H.; Mazzucato, E.; McKemey, A.K.; Meadows, B.T.; Messner, R.; Mockett, P.M.; Moffeit, K.C.; Mours, B.; Mueller, G.; Muller, D.; Nagamine, T.; Nauenberg, U.; Neal, H.; Nussbaum, M.; Ohnishi, Y.; Osborne, L.S.; Panvini, R.S.; Park, H.; Pavel, T.J.; Peruzzi, I.; Piccolo, M.; Piemontese, L.; Pieroni, E.; Pitts, K.T.; Plano, R.J.; Prepost, R.; Prescott, C.Y.; Punkar, G.D.; Quigley, J.; Ratcliff, B.N.; Reeves, T.W.; Reidy, J.; Rensing, P.E.; Rochester, L.S.; Rothberg, J.E.; Rowson, P.C.; (The SLD Collabor..

    1995-11-01

    A measurement of the lifetime of the {tau} lepton has been made using a sample of 1671 {ital Z}{sup 0}{r_arrow}{tau}{sup +}{tau}{sup {minus}} decays collected by the SLD detector at the SLC. The measurement benefits from the small and stable collision region at the SLC and the precision pixel vertex detector of the SLD. Three analysis techniques have been used: decay length, impact parameter, and impact parameter difference methods. The combined result is {tau}{sub {tau}}=297{plus_minus}9 (stat){plus_minus}5(syst) fs.

  19. Improved Limits on the Lepton Flavor Violating Decays Tau -> l V^0

    SciTech Connect

    Aubert, B.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; /LBL, Berkeley /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT, LNS /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /INFN, Naples /Naples U. /INFN, Naples /INFN, Naples /Naples U. /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /Pennsylvania U. /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Stanford U., Phys. Dept. /SUNY, Albany /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Trieste /Trieste U. /Valencia U., IFIC /Victoria U. /Warwick U. /Wisconsin U., Madison

    2009-06-19

    The authors search for the neutrinoless, lepton-flavor-violating tau decays {tau}{sup -} {yields} {ell}{sup -}V{sup 0}, where {ell} is an electron or muon and V{sup 0} is a fector meson reconstructed as {phi} {yields} K{sup +}K{sup -}, {rho} {yields} {pi}{sup +}{pi}{sup -}, K* {yields} K{sup +}{pi}{sup -}, {bar K}* {yields} K{sup -}{pi}{sup +}. The analysis has been performed using 451 fb{sup -1} of data collected at an e{sup +}e{sup -} center-of-mass energy near 10.58 GeV with the BABAR detector at the PEP-II storage rings. The number of events found in the data is compatible with the background expectation, and upper limits on the branching fractions are set in the range (2.6-19) x 10{sup -8} at the 90% confidence level.

  20. B ---> mu mu and B ---> tau nu decays

    SciTech Connect

    Scuri, Fabrizio; /INFN, Pisa

    2009-01-01

    An overview of the most recent experimental results on Branching Fractions of rare fully leptonic B decays is given; constraints on the parameters of some New Physics models are presented. Perspectives with new accelerator programs are discussed.

  1. Tau immunotherapy and imaging.

    PubMed

    Sigurdsson, Einar M

    2014-01-01

    Disappointing findings from recent phase III trials on amyloid-? (A?) immunotherapy for Alzheimer's disease (AD) have shifted the focus of such treatments to the tau protein. As tau pathology correlates better with the degree of dementia than A? plaque burden, it is a more attractive target once cognitive impairments are evident, while A? therapies may be better suited for the presymptomatic phase of the disease. Over 12 years ago, we initiated a tau immunotherapy program, seeking to alleviate the functional impairments associated with tau lesions in tauopathies. We have reported that various active and passive tau immunizations diminish tau pathology and improve function, including cognition, in different mouse models. Both extra- and intracellular pathways are likely involved. The antibodies may block the spread of tau pathology via microglial phagocytosis of the antibody-tau complex and facilitate lysosomal tau clearance in neurons after endosomal uptake. We have observed such antibody internalization following intracarotid injection in mice and in various culture models. These include brain slices and primary neurons from tangle mice as well as human neuroblastoma cell lines. Antibody targeting of different intracellular protein aggregates, including ?-synuclein, A? and superoxide dismutase has been reported by others. Now, several laboratories have confirmed and extended our findings using various active and passive tau immunizations in different models, thereby clearly establishing the feasibility of this approach for clinical trials. We are also working on imaging approaches to monitor tau pathology, its consequences and the efficacy of treatments. Dire need exists for such diagnostic methods for tauopathies. Overall, therapies and diagnostic tools targeting tau pathology have a great potential for AD and other tauopathies. PMID:24029727

  2. Improved limits on the lepton-flavor violating decays tau{-}-->l{-}l{+}l{-}.

    PubMed

    Aubert, B; Bona, M; Boutigny, D; Karyotakis, Y; Lees, J P; Poireau, V; Prudent, X; Tisserand, V; Zghiche, A; Garra Tico, J; Grauges, E; Lopez, L; Palano, A; Pappagallo, M; Eigen, G; Stugu, B; Sun, L; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Osipenkov, I L; Ronan, M T; Tackmann, K; Tanabe, T; Wenzel, W A; Del Amo Sanchez, P; Hawkes, C M; Watson, A T; Koch, H; Schroeder, T; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Mattison, T S; McKenna, J A; Barrett, M; Khan, A; Saleem, M; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Bondioli, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Martin, E C; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Liu, F; Long, O; Shen, B C; Vitug, G M; Zhang, L; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Schalk, T; Schumm, B A; Seiden, A; Wilson, M G; Winstrom, L O; Chen, E; Cheng, C H; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Andreassen, R; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Gabareen, A M; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Wacker, K; Klose, V; Kobel, M J; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Lombardo, V; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Watson, J E; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cecchi, A; Cibinetto, G; Franchini, P; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Santoro, V; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Chaisanguanthum, K S; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Dauncey, P D; Flack, R L; Nash, J A; Panduro Vazquez, W; Tibbetts, M; Behera, P K; Chai, X; Charles, M J; Mallik, U; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gao, Y Y; Gritsan, A V; Guo, Z J; Lae, C K; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Bquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Sordini, V; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Bingham, I; Burke, J P; Chavez, C A; Fry, J R; Gabathuler, E; Gamet, R; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; George, K A; Di Lodovico, F; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Paramesvaran, S; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Bailey, D; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; West, T J; Yi, J I; Anderson, J; Chen, C; Jawahery, A; Roberts, D A; Simi, G; Tuggle, J M; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Salvati, E; Saremi, S; Cowan, R; Dujmic, D; Fisher, P H; Koeneke, K; Sciolla, G; Spitznagel, M; Taylor, F; Yamamoto, R K; Zhao, M; Zheng, Y; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; De Nardo, G; Fabozzi, F; Lista, L; Monorchio, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Knoepfel, K J; Losecco, J M; Benelli, G; Corwin, L A; Honscheid, K; Kagan, H; Kass, R; Morris, J P; Rahimi, A M; Regensburger, J J; Sekula, S J; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gagliardi, N; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Ben-Haim, E; Briand, H; Calderini, G; Chauveau, J; David, P; Del Buono, L; de la Vaissire, Ch; Hamon, O; Leruste, Ph; Malcls, J; Ocariz, J; Perez, A; Prendki, J; Gladney, L; Biasini, M; Covarelli, R; Manoni, E; Angelini, C; Batignani, G; Bettarini, S; Carpinelli, M; Cenci, R; Cervelli, A; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G

    2007-12-21

    A search for the neutrinoless, lepton-flavor violating decay of the tau lepton into three charged leptons has been performed using 376 fb{-1} of data collected at an e{+}e{-} center-of-mass energy around 10.58 GeV with the BABAR detector at the SLAC PEP-II storage rings. In all six decay modes considered, the numbers of events found in data are compatible with the background expectations. Upper limits on the branching fractions are set in the range (4-8)x10{-8} at 90% confidence level. PMID:18233515

  3. Search for lepton-flavor violation in the decay tau- --> l- l+ l-.

    PubMed

    Aubert, B; Barate, R; Boutigny, D; Couderc, F; Gaillard, J-M; Hicheur, A; Karyotakis, Y; Lees, J P; Tisserand, V; Zghiche, A; Palano, A; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Borgland, A W; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; LeClerc, C; Levi, M E; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Shelkov, V G; Telnov, A V; Wenzel, W A; Ford, K; Harrison, T J; Hawkes, C M; Morgan, S E; Watson, A T; Watson, N K; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Steinke, M; Boyd, J T; Chevalier, N; Cottingham, W N; Kelly, M P; Latham, T E; Wilson, F F; Abe, K; Cuhadar-Donszelmann, T; Hearty, C; Mattison, T S; McKenna, J A; Thiessen, D; Kyberd, P; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Ivanchenko, V N; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bruinsma, M; Chao, M; Eschrich, I; Kirkby, D; Lankford, A J; Mandelkern, M; Mommsen, R K; Roethel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Gary, J W; Shen, B C; Wang, K; Del Re, D; Hadavand, H K; Hill, E J; MacFarlane, D B; Paar, H P; Rahatlou, Sh; Sharma, V; Berryhill, J W; Campagnari, C; Dahmes, B; Levy, S L; Long, O; Lu, A; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Heusch, C A; Lockman, W S; Schalk, T; Schmitz, R E; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Yang, S; Jayatilleke, S; Mancinelli, G; Meadows, B T; Sokoloff, M D; Abe, T; Blanc, F; Bloom, P; Chen, S; Clark, P J; Ford, W T; Nauenberg, U; Olivas, A; Rankin, P; Smith, J G; Van Hoek, W C; Zhang, L; Harton, J L; Hu, T; Soffer, A; Toki, W H; Wilson, R J; Altenburg, D; Brandt, T; Brose, J; Colberg, T; Dickopp, M; Feltresi, E; Hauke, A; Lacker, H M; Maly, E; Müller-Pfefferkorn, R; Nogowski, R; Otto, S; Schubert, J; Schubert, K R; Schwierz, R; Spaan, B; Bernard, D; Bonneaud, G R; Brochard, F; Grenier, P; Thiebaux, Ch; Vasileiadis, G; Verderi, M; Bard, D J; Khan, A; Lavin, D; Muheim, F; Playfer, S; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Sarti, A; Treadwell, E; Baldini-Ferroli, R; Calcaterra, A; De Sangro, R; Finocchiaro, G; Patteri, P; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Crosetti, G; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Bailey, S; Brandenburg, G; Morii, M; Won, E; Dubitzky, R S; Langenegger, U; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Gaillard, J R; Morton, G W; Nash, J A; Taylor, G P; Grenier, G J; Lee, S-J; Mallik, U; Cochran, J; Crawley, H B; Lamsa, J; Meyer, W T; Prell, S; Rosenberg, E I; Yi, J; Davier, M; Grosdidier, G; Höcker, A; Laplace, S; Le Diberder, F; Lepeltier, V; Lutz, A M; Petersen, T C; Plaszczynski, S; Schune, M H; Tantot, L; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Coleman, J P; Fry, J R; Gabathuler, E; Gamet, R; Kay, M; Parry, R J; Payne, D J; Sloane, R J; Touramanis, C; Back, J J; Harrison, P F; Mohanty, G B; Brown, C L; Cowan, G; Flack, R L; Flaecher, H U; George, S; Green, M G; Kurup, A; Marker, C E; McMahon, T R; Ricciardi, S; Salvatore, F; Vaitsas, G; Winter, M A; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Hart, P A; Hodgkinson, M C; Lafferty, G D; Lyon, A J; Williams, J C; Farbin, A; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Lillard, V; Roberts, D A; Blaylock, G; Dallapiccola, C; Flood, K T; Hertzbach, S S; Kofler, R; Koptchev, V B; Moore, T B; Saremi, S; Staengle, H; Willocq, S; Cowan, R; Sciolla, G; Taylor, F; Yamamoto, R K; Mangeol, D J J; Patel, P M; Robertson, S H; Lazzaro, A; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Taras, P; Nicholson, H; Cartaro, C; Cavallo, N; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M; Raven, G; Wilden, L; Jessop, C P; LoSecco, J M; Gabriel, T A; Allmendinger, T; Brau, B; Gan, K K; Honscheid, K; Hufnagel, D; Kagan, H; Kass, R; Pulliam, T; Ter-Antonyan, R; Wong, Q K; Brau, J; Frey, R; Igonkina, O; Potter, C T; Sinev, N B; Strom, D; Torrence, E; Colecchia, F; Dorigo, A; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Tiozzo, G; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; de la Vaissière, Ch; Del Buono, L; Hamon, O; John, M J J; Leruste, Ph; Ocariz, J; Pivk, M; Roos, L; T'Jampens, S; Therin, G; Manfredi, P F; Re, V; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Anulli, F; Biasini, M; Peruzzi, I M; Pioppi, M; Angelini, C; Batignani, G; Bettarini, S; Bondioli, M; Bucci, F; Calderini, G; Carpinelli, M; Del Gamba, V; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Martinez-Vidal, F; Morganti, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Sandrelli, F; Walsh, J; Haire, M; Judd, D; Paick, K; Wagoner, D E; Danielson, N; Elmer, P; Lu, C; Miftakov, V; Olsen, J; Smith, A J S; Varnes, E W; Bellini, F; Cavoto, G; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Pierini, M; Piredda, G; Safai Tehrani, F; Voena, C; Christ, S; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Geddes, N I; Gopal, G P; Olaiya, E O; Xella, S M; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Giraud, P-F; Hamel de Monchenault, G; Kozanecki, W; Langer, M; Legendre, M; London, G W; Mayer, B; Schott, G; Vasseur, G; Yèche, Ch; Zito, M; Purohit, M V; Weidemann, A W; Yumiceva, F X; Aston, D; Bartoldus, R; Berger, N; Boyarski, A M; Buchmueller, O L; Convery, M R; Cristinziani, M; De Nardo, G; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W; Elsen, E E; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Luth, V; Lynch, H L; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Petrak, S; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Simi, G; Snyder, A; Soha, A; Stelzer, J; Su, D; Sullivan, M K; Va'vra, J; Wagner, S R; Weaver, M; Weinstein, A J R; Wisniewski, W J; Wittgen, M; Wright, D H; Young, C C; Burchat, P R; Edwards, A J; Meyer, T I; Petersen, B A; Roat, C; Ahmed, S; Alam, M S; Ernst, J A; Saeed, M A; Saleem, M; Wappler, F R; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Kim, H; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bona, M; Gallo, F; Gamba, D; Borean, C; Bosisio, L; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Poropat, P; Vitale, L; Vuagnin, G; Panvini, R S; Banerjee, Sw; Brown, C M; Fortin, D; Jackson, P D; Kowalewski, R; Roney, J M; Band, H R; Dasu, S; Datta, M; Eichenbaum, A M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Di Lodovico, F; Mihalyi, A; Mohapatra, A K; Pan, Y; Prepost, R; Sekula, S J; Tan, P; von Wimmersperg-Toeller, J H; Wu, J; Wu, S L; Yu, Z; Neal, H

    2004-03-26

    A search for the lepton-flavor-violating decay of the tau into three charged leptons has been performed using 91.5 fb(-1) of data collected at an e(+)e(-)center-of-mass energy around 10.58 GeV with the BABAR detector at the SLAC storage ring PEP-II. In all six decay modes considered, the numbers of events found in data are compatible with the background expectations. Upper limits on the branching fractions are set in the range (1-3)x10(-7) at 90% confidence level. PMID:15089664

  4. Limits on tau lepton flavor violating decays in three charged leptons

    SciTech Connect

    Cervelli, Alberto

    2010-04-29

    A search for the neutrinoless, lepton-flavor violating decay of the {tau} lepton into three charged leptons has been performed using an integrated luminosity of 468 fb{sup -1} collected with the BABAR detector at the PEP-II collider. In all six decay modes considered, the numbers of events found in data are compatible with the background expectations. Upper limits on the branching fractions are set in the range (1.8-3.3) x 10{sup -8} at 90% confidence level.

  5. Selected Topics in Tau Physics from BaBar

    SciTech Connect

    Paramesvaran, S.; /Royal Holloway, U. of London

    2012-04-06

    Selected results from {tau} analyses performed using the BABAR detector at the SLAC National Accelerator Laboratory are presented. A precise measurement of the {tau} mass and the {tau}{sup +}{tau}{sup -} mass difference is undertaken using the hadronic decay mode {tau}{sup {+-}} {yields} {pi}{sup +}{pi}{sup -}{pi}{sup {+-}}{nu}{sub {tau}}. In addition an investigation into the strange decay modes {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{pi}{sup 0}{nu}{sub {tau}} and {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{nu}{sub {tau}} is also presented, including a fit to the {tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{nu}{sub {tau}} invariant mass spectrum. Precise values for M(K*(892)) and {Lambda}(K*(892)) are obtained.

  6. Majoron emission in muon and tau decays revisited

    NASA Astrophysics Data System (ADS)

    Hirsch, M.; Meyer, J.; Porod, W.; Vicente, A.

    2009-03-01

    In models where the breaking of lepton number is spontaneous a massless Goldstone boson, the Majoron (J), appears. We calculate the theoretically allowed range for the branching ratios of Majoron-emitting charged lepton decays, such as Br(??eJ) and Br(??eJ?), in a supersymmetric model with spontaneous breaking of R-parity. Br(??eJ) is maximal in the same region of parameter space for which the lightest neutralino decays mainly invisibly. A measurement of Br(??eJ) thus potentially provides information on R-parity violation complementary to accelerator searches. We also briefly discuss existing bounds and prospects for future improvements on the Majoron coupling to charged leptons.

  7. Measurement of the tau lifetime

    SciTech Connect

    Jaros, J.A.

    1982-10-01

    If the tau lepton couples to the charged weak current with universal strength, its lifetime can be expressed in terms of the muon's lifetime, the ratio of the masses of the muon and the tau, and the tau's branching ratio into e anti nu/sub e/ nu/sub tau/ as tau/sub tau/ = tau/sub ..mu../ (m/sub ..mu..//m/sub tau/)/sup 5/ B(tau ..-->.. e anti nu/sub e/nu/sub tau/) = 2.8 +- 0.2 x 10/sup -13/ s. This paper describes the measurement of the tau lifetime made by the Mark II collaboration, using a new high precision drift chamber in contunction with the Mark II detector at PEP. The results of other tau lifetime measurements are summarized.

  8. Reconstruction and identification of $\\tau$ lepton decays to hadrons and $\

    SciTech Connect

    Khachatryan, Vardan

    2015-10-27

    This paper describes the algorithms used by the CMS experiment to reconstruct and identify τ→ hadrons + vt decays during Run 1 of the LHC. The performance of the algorithms is studied in proton-proton collisions recorded at a centre-of-mass energy of 8 TeV, corresponding to an integrated luminosity of 19.7 fb-1. The algorithms achieve an identification efficiency of 50–60%, with misidentification rates for quark and gluon jets, electrons, and muons between per mille and per cent levels.

  9. Search for CP Violation in {tau}{sup {+-}}{yields}K{sub S}{sup 0}{pi}{sup {+-}}{nu}{sub {tau}} Decays at Belle

    SciTech Connect

    Bischofberger, M.; Hayashii, H.; Miyabayashi, K.; Adamczyk, K.; Bozek, A.; Aihara, H.; Aulchenko, V.; Eidelman, S.; Epifanov, D.; Shwartz, B.; Vinokurova, A.; Zhulanov, V.; Bakich, A. M.; McOnie, S.; Balagura, V.; Danilov, M.; Mizuk, R.; Pakhlova, G.; Uglov, T.; Barberio, E.

    2011-09-23

    We report on a search for CP violation in {tau}{sup {+-}}{yields}K{sub S}{sup 0}{pi}{sup {+-}}{nu}{sub {tau}} decays using a data sample of 699 fb{sup -1} collected by the Belle experiment at the KEKB electron-positron asymmetric-energy collider. The CP asymmetry is measured in four bins of the invariant mass of the K{sub S}{sup 0}{pi}{sup {+-}} system and found to be compatible with zero with a precision of O(10{sup -3}) in each mass bin. Limits for the CP violation parameter Im({eta}{sub S}) are given at the 90% confidence level. These limits are |Im({eta}{sub S})|<0.026 or better, depending on the parametrization used to describe the hadronic form factors, and improve upon previous limits by 1 order of magnitude.

  10. Deletion of murine tau gene increases tau aggregation in a human mutant tau transgenic mouse model.

    PubMed

    Ando, Kunie; Leroy, Karelle; Heraud, Cline; Kabova, Anna; Yilmaz, Zehra; Authelet, Michle; Suain, Valrie; De Decker, Robert; Brion, Jean-Pierre

    2010-08-01

    We have reported previously a tau transgenic mouse model (Tg30tau) overexpressing human 4R1N double-mutant tau (P301S and G272V) and that develops AD (Alzheimer's disease)-like NFTs (neurofibrillary tangles) in an age-dependent manner. Since murine tau might interfere with the toxic effects of human mutant tau, we set out to analyse the phenotype of our Tg30tau model in the absence of endogenous murine tau with the aim to reproduce more faithfully a model of human tauopathy. By crossing the Tg30tau line with TauKO (tau-knockout) mice, we have obtained a new mouse line called Tg30xTauKO that expresses only exogenous human double-mutant 4R1N tau. Whereas Tg30xTauKO mice express fewer tau proteins compared with Tg30tau, they exhibit augmented sarkosyl-insoluble tau in the brain and an increased number of Gallyas-positive NFTs in the hippocampus. Taken together, exclusion of murine tau causes accelerated tau aggregation during aging of this mutant tau transgenic model. PMID:20658993

  11. Tau in physiology and pathology.

    PubMed

    Wang, Yipeng; Mandelkow, Eckhard

    2016-01-01

    Tau is a microtubule-associated protein that has a role in stabilizing neuronal microtubules and thus in promoting axonal outgrowth. Structurally, tau is a natively unfolded protein, is highly soluble and shows little tendency for aggregation. However, tau aggregation is characteristic of several neurodegenerative diseases known as tauopathies. The mechanisms underlying tau pathology and tau-mediated neurodegeneration are debated, but considerable progress has been made in the field of tau research in recent years, including the identification of new physiological roles for tau in the brain. Here, we review the expression, post-translational modifications and functions of tau in physiology and in pathophysiology. PMID:26631930

  12. Search for the Baryon and Lepton Number Violating Decays tau to Lambda h

    SciTech Connect

    Aubert, B.

    2006-11-28

    The authors have searched for the violation of baryon number B and lepton number L in the (B-L)-conserving modes {tau}{sup -} {yields} {bar {Lambda}}{sup 0}{pi}{sup -} and {tau}{sup -} {yields} {bar {Lambda}}{sup 0}K{sup -} as well as the (B-L)-violating modes {tau}{sup -} {yields} {Lambda}{sup 0}{pi}{sup -} and {tau}{sup -} {yields} {Lambda}{sup 0}K{sup -} using 237 fb{sup -1} of data collected with the BABAR detector at the PEP-II asymmetric-energy e{sup +}e{sup -} storage ring. They do not observe any signal and determine preliminary upper limits on the branching fractions {Beta}({tau}{sup -} {yields} {bar {Lambda}}{sup 0}{pi}{sup -}) < 5.9 x 10{sup -8}, {Beta}({tau}{sup -} {yields} {Lambda}{sup 0}{pi}{sup -}) < 5.8 x 10{sup -8}, {Beta}({tau}{sup -} {yields} {bar {Lambda}}{sup 0}K{sup -}) < 7.2 x 10{sup -8}, and {Beta}({tau}{sup -} {yields} {Lambda}{sup 0}K{sup -}) < 15 x 10{sup -8} at 90% confidence level.

  13. Four-pion production in {tau} decays and e{sup +}e{sup -} annihilation: An update

    SciTech Connect

    Czyz, Henryk; Kuehn, Johann H.; Wapienik, Agnieszka

    2008-06-01

    An improved description of four-pion production in electron-positron annihilation and in {tau}-lepton decays is presented. The model amplitude is fitted to recent data from BABAR which cover a wide energy range and which were obtained exploiting the radiative return. Predicting {tau}-decay distributions from e{sup +}e{sup -} data and comparing these predictions with ALEPH and CLEO results, the validity of isospin symmetry is confirmed within the present experimental errors. A good description of two- and three-pion subdistributions is obtained. Special emphasis is put on the predictions for {omega}{pi}({yields}{pi}{sup +}{pi}{sup -}{pi}{sup 0}) in e{sup +}e{sup -} annihilation and in {tau} decay. The model amplitude is implemented in the Monte Carlo generator PHOKHARA.

  14. Pfaffian and Determinantal Tau Functions

    NASA Astrophysics Data System (ADS)

    van de Leur, Johan W.; Orlov, Alexander Yu.

    2015-11-01

    Adler, Shiota and van Moerbeke observed that a tau function of the Pfaff lattice is a square root of a tau function of the Toda lattice hierarchy of Ueno and Takasaki. In this paper, we give a representation theoretical explanation for this phenomenon. We consider 2-BKP and two-component 2-KP tau functions. We shall show that a square of a BKP tau function is equal to a certain two-component KP tau function and a square of a 2-BKP tau function is equal to a certain two-component 2-KP tau function.

  15. Search for the associated production of a b quark and a neutral supersymmetric Higgs boson that decays into tau pairs.

    PubMed

    Abazov, V M; Abbott, B; Abolins, M; Acharya, B S; Adams, M; Adams, T; Aguilo, E; Ahsan, M; Alexeev, G D; Alkhazov, G; Alton, A; Alverson, G; Alves, G A; Ancu, L S; Aoki, M; Arnoud, Y; Arov, M; Askew, A; Asman, B; Atramentov, O; Avila, C; BackusMayes, J; Badaud, F; Bagby, L; Baldin, B; Bandurin, D V; Banerjee, S; Barberis, E; Barfuss, A-F; Baringer, P; Barreto, J; Bartlett, J F; Bassler, U; Bauer, D; Beale, S; Bean, A; Begalli, M; Begel, M; Belanger-Champagne, C; Bellantoni, L; Benitez, J A; Beri, S B; Bernardi, G; Bernhard, R; Bertram, I; Besançon, M; Beuselinck, R; Bezzubov, V A; Bhat, P C; Bhatnagar, V; Blazey, G; Blessing, S; Bloom, K; Boehnlein, A; Boline, D; Bolton, T A; Boos, E E; Borissov, G; Bose, T; Brandt, A; Brock, R; Brooijmans, G; Bross, A; Brown, D; Bu, X B; Buchholz, D; Buehler, M; Buescher, V; Bunichev, V; Burdin, S; Burnett, T H; Buszello, C P; Calfayan, P; Calpas, B; Calvet, S; Camacho-Pérez, E; Cammin, J; Carrasco-Lizarraga, M A; Carrera, E; Carvalho, W; Casey, B C K; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K M; Chandra, A; Cheu, E; Chevalier-Théry, S; Cho, D K; Cho, S W; Choi, S; Choudhary, B; Christoudias, T; Cihangir, S; Claes, D; Clutter, J; Cooke, M; Cooper, W E; Corcoran, M; Couderc, F; Cousinou, M-C; Cutts, D; Cwiok, M; Das, A; Davies, G; De, K; de Jong, S J; De la Cruz-Burelo, E; DeVaughan, K; Déliot, F; Demarteau, M; Demina, R; Denisov, D; Denisov, S P; Desai, S; Diehl, H T; Diesburg, M; Dominguez, A; Dorland, T; Dubey, A; Dudko, L V; Duflot, L; Duggan, D; Duperrin, A; Dutt, S; Dyshkant, A; Eads, M; Edmunds, D; Ellison, J; Elvira, V D; Enari, Y; Eno, S; Evans, H; Evdokimov, A; Evdokimov, V N; Facini, G; Ferapontov, A V; Ferbel, T; Fiedler, F; Filthaut, F; Fisher, W; Fisk, H E; Fortner, M; Fox, H; Fuess, S; Gadfort, T; Galea, C F; Garcia-Bellido, A; Gavrilov, V; Gay, P; Geist, W; Geng, W; Gerbaudo, D; Gerber, C E; Gershtein, Y; Gillberg, D; Ginther, G; Golovanov, G; Gómez, B; Goussiou, A; Grannis, P D; Greder, S; Greenlee, H; Greenwood, Z D; Gregores, E M; Grenier, G; Gris, Ph; Grivaz, J-F; Grohsjean, A; Grünendahl, S; Grünewald, M W; Guo, F; Guo, J; Gutierrez, G; Gutierrez, P; Haas, A; Haefner, P; Hagopian, S; Haley, J; Hall, I; Hall, R E; Han, L; Harder, K; Harel, A; Hauptman, J M; Hays, J; Hebbeker, T; Hedin, D; Hegeman, J G; Heinson, A P; Heintz, U; Hensel, C; Heredia-De la Cruz, I; Herner, K; Hesketh, G; Hildreth, M D; Hirosky, R; Hoang, T; Hobbs, J D; Hoeneisen, B; Hohlfeld, M; Hossain, S; Houben, P; Hu, Y; Hubacek, Z; Huske, N; Hynek, V; Iashvili, I; Illingworth, R; Ito, A S; Jabeen, S; Jaffré, M; Jain, S; Jakobs, K; Jamin, D; Jesik, R; Johns, K; Johnson, C; Johnson, M; Johnston, D; Jonckheere, A; Jonsson, P; Juste, A; Kajfasz, E; Karmanov, D; Kasper, P A; Katsanos, I; Kaushik, V; Kehoe, R; Kermiche, S; Khalatyan, N; Khanov, A; Kharchilava, A; Kharzheev, Y N; Khatidze, D; Kirby, M H; Kirsch, M; Kohli, J M; Kozelov, A V; Kraus, J; Kumar, A; Kupco, A; Kurca, T; Kuzmin, V A; Kvita, J; Lacroix, F; Lam, D; Lammers, S; Landsberg, G; Lebrun, P; Lee, H S; Lee, W M; Leflat, A; Lellouch, J; Li, L; Li, Q Z; Lietti, S M; Lim, J K; Lincoln, D; Linnemann, J; Lipaev, V V; Lipton, R; Liu, Y; Liu, Z; Lobodenko, A; Lokajicek, M; Love, P; Lubatti, H J; Luna-Garcia, R; Lyon, A L; Maciel, A K A; Mackin, D; Mättig, P; Magaña-Villalba, R; Mal, P K; Malik, S; Malyshev, V L; Maravin, Y; Martin, B; Martínez-Ortega, J; McCarthy, R; McGivern, C L; Meijer, M M; Melnitchouk, A; Mendoza, L; Menezes, D; Mercadante, P G; Merkin, M; Meyer, A; Meyer, J; Mondal, N K; Moore, R W; Moulik, T; Muanza, G S; Mulhearn, M; Mundal, O; Mundim, L; Nagy, E; Naimuddin, M; Narain, M; Nayyar, R; Neal, H A; Negret, J P; Neustroev, P; Nilsen, H; Nogima, H; Novaes, S F; Nunnemann, T; Obrant, G; Onoprienko, D; Orduna, J; Osman, N; Osta, J; Otec, R; Otero y Garzón, G J; Owen, M; Padilla, M; Padley, P; Pangilinan, M; Parashar, N; Parihar, V; Park, S-J; Park, S K; Parsons, J; Partridge, R; Parua, N; Patwa, A; Penning, B; Perfilov, M; Peters, K; Peters, Y; Pétroff, P; Piegaia, R; Piper, J; Pleier, M-A; Podesta-Lerma, P L M; Podstavkov, V M; Pogorelov, Y; Pol, M-E; Polozov, P; Popov, A V; Prewitt, M; Protopopescu, S; Qian, J; Quadt, A; Quinn, B; Rangel, M S; Ranjan, K; Ratoff, P N; Razumov, I; Renkel, P; Rich, P; Rijssenbeek, M; Ripp-Baudot, I; Rizatdinova, F; Robinson, S; Rominsky, M; Royon, C; Rubinov, P; Ruchti, R; Safronov, G; Sajot, G; Sánchez-Hernández, A; Sanders, M P; Sanghi, B; Savage, G; Sawyer, L; Scanlon, T; Schaile, D; Schamberger, R D; Scheglov, Y; Schellman, H; Schliephake, T; Schlobohm, S; Schwanenberger, C; Schwienhorst, R; Sekaric, J; Severini, H; Shabalina, E; Shamim, M; Shary, V; Shchukin, A A; Shivpuri, R K; Simak, V; Sirotenko, V; Skubic, P; Slattery, P; Smirnov, D; Snow, G R; Snow, J; Snyder, S; Söldner-Rembold, S; Sonnenschein, L; Sopczak, A; Sosebee, M; Soustruznik, K; Spurlock, B; Stark, J; Stolin, V; Stoyanova, D A; Strandberg, J; Strang, M A; Strauss, E; Strauss, M; Ströhmer, R; Strom, D; Stutte, L; Sumowidagdo, S; Svoisky, P; Takahashi, M; Tanasijczuk, A; Taylor, W; Tiller, B; Titov, M; Tokmenin, V V; Torchiani, I; Tsybychev, D; Tuchming, B; Tully, C; Tuts, P M; Unalan, R; Uvarov, L; Uvarov, S; Uzunyan, S; van den Berg, P J; Van Kooten, R; van Leeuwen, W M; Varelas, N; Varnes, E W; Vasilyev, I A; Verdier, P; Vertogradov, L S; Verzocchi, M; Vesterinen, M; Vilanova, D; Vint, P; Vokac, P; Wagner, R; Wahl, H D; Wang, M H L S; Warchol, J; Watts, G; Wayne, M; Weber, G; Weber, M; Wenger, A; Wetstein, M; White, A; Wicke, D; Williams, M R J; Wilson, G W; Wimpenny, S J; Wobisch, M; Wood, D R; Wyatt, T R; Xie, Y; Xu, C; Yacoob, S; Yamada, R; Yang, W-C; Yasuda, T; Yatsunenko, Y A; Ye, Z; Yin, H; Yip, K; Yoo, H D; Youn, S W; Yu, J; Zeitnitz, C; Zelitch, S; Zhao, T; Zhou, B; Zhu, J; Zielinski, M; Zieminska, D; Zivkovic, L; Zutshi, V; Zverev, E G

    2010-04-16

    We report results from a search for production of a neutral Higgs boson in association with a b quark. We search for Higgs decays to tau pairs with one tau subsequently decaying to a muon and the other to hadrons. The data correspond to 2.7 fb(-1) of pp collisions recorded by the D0 detector at square root(s)=1.96 TeV. The data are found to be consistent with background predictions. The result allows us to exclude a significant region of parameter space of the minimal supersymmetric model. PMID:20481981

  16. Search for lepton-flavor and lepton-number violation in the decay tau(-) -->l-(+)h+(-)h'(-).

    PubMed

    Aubert, B; Barate, R; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Pappagallo, M; Pompili, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Breon, A B; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Day, C T; Gill, M S; Gritsan, A V; Groysman, Y; Jacobsen, R G; Kadel, R W; Kadyk, J; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lynch, G; Mir, L M; Oddone, P J; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Morgan, S E; Watson, A T; Fritsch, M; Goetzen, K; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Chevalier, N; Cottingham, W N; Kelly, M P; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Teodorescu, L; Blinov, A E; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Kravchenko, E A; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Yushkov, A N; Best, D; Bondioli, M; Bruinsma, M; Chao, M; Eschrich, I; Kirkby, D; Lankford, A J; Mandelkern, M; Mommsen, R K; Roethel, W; Stoker, D P; Buchanan, C; Hartfiel, B L; Weinstein, A J R; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; del Re, D; Hadavand, H K; Hill, E J; MacFarlane, D B; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Mazur, M A; Richman, J D; Verkerke, W; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Dubois-Felsmann, G P; Dvoretskii, A; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Ryd, A; Samuel, A; Andreassen, R; Jayatilleke, S; Mancinelli, G; Meadows, B T; Sokoloff, M D; Blanc, F; Bloom, P; Chen, S; Ford, W T; Nauenberg, U; Olivas, A; Rankin, P; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Zeng, Q; Altenburg, D; Feltresi, E; Hauke, A; Spaan, B; Brandt, T; Brose, J; Dickopp, M; Klose, V; Lacker, H M; Nogowski, R; Otto, S; Petzold, A; Schott, G; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Bernard, D; Bonneaud, G R; Grenier, P; Schrenk, S; Thiebaux, Ch; Vasileiadis, G; Verderi, M; Bard, D J; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Xie, Y; Andreotti, M; Azzolini, V; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Piemontese, L; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Patteri, P; Peruzzi, I M; Piccolo, M; Zallo, A; Buzzo, A; Capra, R; Contri, R; Lo Vetere, M; Macri, M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Bailey, S; Brandenburg, G; Chaisanguanthum, K S; Morii, M; Won, E; Wu, J; Dubitzky, R S; Langenegger, U; Marks, J; Schenk, S; Uwer, U; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Gaillard, J R; Morton, G W; Nash, J A; Nikolich, M B; Taylor, G P; Vazquez, W P; Charles, M J; Mader, W F; Mallik, U; Mohapatra, A K; Cochran, J; Crawley, H B; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Yi, J; Arnaud, N; Davier, M; Giroux, X; Grosdidier, G; Höcker, A; Le Diberder, F; Lepeltier, V; Lutz, A M; Oyanguren, A; Petersen, T C; Pierini, M; Plaszczynski, S; Rodier, S; Roudeau, P; Schune, M H; Stocchi, A; Wormser, G; Cheng, C H; Lange, D J; Simani, M C; Wright, D M; Bevan, A J; Chavez, C A; Coleman, J P; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Parry, R J; Payne, D J; Schofield, K C; Touramanis, C; Cormack, C M; Di Lodovico, F; Sacco, R; Brown, C L; Cowan, G; Flaecher, H U; Green, M G; Hopkins, D A; Jackson, P S; McMahon, T R; Ricciardi, S; Salvatore, F; Brown, D; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Hodgkinson, M C; Lafferty, G D; Naisbit, M T; Williams, J C; Chen, C; Farbin, A; Hulsbergen, W D; Jawahery, A; Kovalskyi, D; Lae, C K; Lillard, V; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Kofler, R; Koptchev, V B; Li, X; Moore, T B; Saremi, S; Staengle, H; Willocq, S; Cowan, R; Koeneke, K; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Reidy, J; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Côté, D; Taras, P; Viaud, B; Nicholson, H; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M; Bulten, H; Raven, G; Snoek, H L; Wilden, L; Jessop, C P; LoSecco, J M; Allmendinger, T; Benelli, G; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Pulliam, T; Rahimi, A M; Ter-Antonyan, R; Wong, Q K; Brau, J; Frey, R; Igonkina, O; Lu, M; Potter, C T; Sinev, N B; Strom, D; Strube, J; Torrence, E; Dorigo, A; Galeazzi, F; Margoni, M; Morandin, M; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H; Chauveau, J; David, P; Del Buono, L; de la Vaissière, Ch; Hamon, O; John, M J J; Leruste, Ph; Malclès, J; Ocariz, J; Roos, L; Therin, G; Behera, P K; Gladney, L; Guo, Q H; Panetta, J; Biasini, M; Covarelli, R; Pacetti, S; Pioppi, M; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Morganti, M; Neri, N; Paoloni, E; Rama, M; Rizzo, G; Walsh, J; Haire, M; Judd, D; Wagoner, D E; Biesiada, J; Danielson, N; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Bellini, F; Cavoto, G; D'Orazio, A; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Tehrani, F Safai; Voena, C; Schröder, H; Wagner, G; Waldi, R; Adye, T; De Groot, N; Franek, B; Gopal, G P; Olaiya, E O; Wilson, F F; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Giraud, P-F; Graziani, G; de Monchenault, G Hamel; Kozanecki, W; Legendre, M; London, G W; Mayer, B; Vasseur, G; Yèche, Ch; Zito, M; Purohit, M V; Weidemann, A W; Wilson, J R; Yumiceva, F X; Abe, T; Allen, M T; Aston, D; Bartoldus, R; Berger, N; Boyarski, A M; Buchmueller, O L; Claus, R; Convery, M R; Cristinziani, M; Dingfelder, J C; Dong, D; Dorfan, J; Dujmic, D; Dunwoodie, W; Fan, S; Field, R C; Glanzman, T; Gowdy, S J; Hadig, T; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Kocian, M L; Leith, D W G S; Libby, J; Luitz, S; Luth, V; Lynch, H L; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Stelzer, J; Su, D; Sullivan, M K; Suzuki, K; Swain, S; Thompson, J M; Va'vra, J; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Roat, C; Ahmed, M; Ahmed, S; Alam, M S; Ernst, J A; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schwitters, R F; Izen, J M; Kitayama, I; Lou, X C; Ye, S; Bianchi, F; Bona, M; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Grancagnolo, S; Lanceri, L; Vitale, L; Martinez-Vidal, F; Panvini, R S; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Eichenbaum, A M; Flood, K T; Graham, M; Hollar, J J; Johnson, J R; Kutter, P E; Li, H; Liu, R; Mellado, B; Mihalyi, A; Pan, Y; Prepost, R; Tan, P; von Wimmersperg-Toeller, J H; Wu, S L; Yu, Z; Neal, H

    2005-11-01

    A search for lepton-flavor and lepton-number violation in the decay of the tau lepton into one charged lepton and two charged hadrons is performed using 221.4 fb(-1) of data collected at an e+e- center-of-mass energy of 10.58 GeV with the BABAR detector at the SLAC PEP-II storage ring. In all 14 decay modes considered, the observed data are compatible with background expectations, and upper limits are set in the range B(tau-->lhh')<(0.7 - 4.8) x 10(-7) at 90% confidence level. PMID:16383973

  17. Search for a low mass Standard Model Higgs boson in the $\\tau-\\tau$ decay channel in $p\\bar{p}$ collisions at $\\sqrt{s}$ = 1.96 TeV

    SciTech Connect

    Aaltonen, T.; Alvarez Gonzalez, B.; Amerio, S.; Amidei, D.; Anastassov, A.; Annovi, A.; Antos, J.; Apollinari, G.; Appel, J.A.; Apresyan, A.; Arisawa, T.; /Waseda U. /Dubna, JINR

    2012-01-01

    We report on a search for the standard model Higgs boson decaying into pairs of {tau} leptons in p{bar p} collisions produced by the Tevatron at {radical}s = 1.96 TeV. The analyzed data sample was recorded by the CDFII detector and corresponds to an integrated luminosity of 6.0 fb{sup -1}. The search is performed in the final state with one {tau} decaying leptonically and the second one identified through its semi-hadronic decay. Since no significant excess is observed, a 95% credibility level upper limit on the production cross section times branching ratio to the {tau}{tau} final state is set for hypothetical Higgs boson masses between 100 and 150 GeV/c{sup 2}. For a Higgs boson of 120 GeV/c{sup 2} the observed (expected) limit is 14.6 (15.3) the predicted value.

  18. Identification and energy calibration of hadronically decaying tau leptons with the ATLAS experiment in pp collisions at √s = 8 TeV

    SciTech Connect

    Aad, G.

    2015-07-02

    This study describes the trigger and offline reconstruction, identification and energy calibration algorithms for hadronic decays of tau leptons employed for the data collected from pp collisions in 2012 with the ATLAS detector at the LHC center-of-mass energy √s=8 TeV. The performance of these algorithms is measured in most cases with Z decays to tau leptons using the full 2012 dataset, corresponding to an integrated luminosity of 20.3 fb–1. An uncertainty on the offline reconstructed tau energy scale of 2–4%, depending on transverse energy and pseudorapidity, is achieved using two independent methods. The offline tau identification efficiency is measured with a precision of 2.5% for hadronically decaying tau leptons with one associated track, and of 4% for the case of three associated tracks, inclusive in pseudorapidity and for a visible transverse energy greater than 20 GeV. For hadronic tau lepton decays selected by offline algorithms, the tau trigger identification efficiency is measured with a precision of 2–8%, depending on the transverse energy. The performance of the tau algorithms, both offline and at the trigger level, is found to be stable with respect to the number of concurrent proton–proton interactions and has supported a variety of physics results using hadronically decaying tau leptons at ATLAS.

  19. Identification and energy calibration of hadronically decaying tau leptons with the ATLAS experiment in pp collisions at √s = 8 TeV

    DOE PAGESBeta

    Aad, G.

    2015-07-02

    This study describes the trigger and offline reconstruction, identification and energy calibration algorithms for hadronic decays of tau leptons employed for the data collected from pp collisions in 2012 with the ATLAS detector at the LHC center-of-mass energy √s=8 TeV. The performance of these algorithms is measured in most cases with Z decays to tau leptons using the full 2012 dataset, corresponding to an integrated luminosity of 20.3 fb–1. An uncertainty on the offline reconstructed tau energy scale of 2–4%, depending on transverse energy and pseudorapidity, is achieved using two independent methods. The offline tau identification efficiency is measured withmore » a precision of 2.5% for hadronically decaying tau leptons with one associated track, and of 4% for the case of three associated tracks, inclusive in pseudorapidity and for a visible transverse energy greater than 20 GeV. For hadronic tau lepton decays selected by offline algorithms, the tau trigger identification efficiency is measured with a precision of 2–8%, depending on the transverse energy. The performance of the tau algorithms, both offline and at the trigger level, is found to be stable with respect to the number of concurrent proton–proton interactions and has supported a variety of physics results using hadronically decaying tau leptons at ATLAS.« less

  20. Tau-tubulin kinase

    PubMed Central

    Ikezu, Seiko; Ikezu, Tsuneya

    2014-01-01

    Tau-tubulin kinase (TTBK) belongs to casein kinase superfamily and phosphorylates microtubule-associated protein tau and tubulin. TTBK has two isoforms, TTBK1 and TTBK2, which contain highly homologous catalytic domains but their non-catalytic domains are distinctly different. TTBK1 is expressed specifically in the central nervous system and is involved in phosphorylation and aggregation of tau. TTBK2 is ubiquitously expressed in multiple tissues and genetically linked to spinocerebellar ataxia type 11. TTBK1 directly phosphorylates tau protein, especially at Ser422, and also activates cycline-dependent kinase 5 in a unique mechanism. TTBK1 protein expression is significantly elevated in Alzheimer’s disease (AD) brains, and genetic variations of the TTBK1 gene are associated with late-onset Alzheimer’s disease in two cohorts of Chinese and Spanish populations. TTBK1 transgenic mice harboring the entire 55-kilobase genomic sequence of human TTBK1 show progression of tau accumulation, neuroinflammation, and neurodegeneration when crossed with tau mutant mice. Our recent study shows that there is a striking switch in mononuclear phagocyte and activation phenotypes in the anterior horn of the spinal cord from alternatively activated (M2-skewed) microglia in P301L tau mutant mice to pro-inflammatory (M1-skewed) infiltrating peripheral monocytes by crossing the tau mice with TTBK1 transgenic mice. TTBK1 is responsible for mediating M1-activated microglia-induced neurotoxicity, and its overexpression induces axonal degeneration in vitro. These studies suggest that TTBK1 is an important molecule for the inflammatory axonal degeneration, which may be relevant to the pathobiology of tauopathy including AD. PMID:24808823

  1. Measurements of the tau Mass and Mass Difference of the tau^+ and tau^- at BABAR

    SciTech Connect

    Aubert, B.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D.N.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /INFN, Naples /Naples U. /INFN, Naples /INFN, Naples /Naples U. /NIKHEF, Amsterdam /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /Pennsylvania U. /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2009-10-30

    The authors present the result of a precision measurement of the mass of the {tau} lepton, M{sub {tau}}, based on 423 fb{sup -1} of data recorded at the {Upsilon}(4S) resonance with the BABAR detector. Using a pseudomass endpoint method, they determine the mass to be 1776.68 {+-} 0.12(stat) {+-} 0.41(syst) MeV. They also measure the mass difference between the {tau}{sup +} and {tau}{sup -}, and obtain (M{sub {tau}{sup +}} - M{sub {tau}{sup -}})/M{sub AVG}{sup {tau}} = (-3.4 {+-} 1.3(stat) {+-} 0.3(syst)) x 10{sup -4}, where M{sub AVG}{sup {tau}} is the average value of M{sub {tau}{sup +}} and M{sub {tau}{sup -}}.

  2. Search for neutral MSSM Higgs bosons decaying to a pair of tau leptons in pp collisions

    SciTech Connect

    Khachatryan, Vardan

    2014-10-28

    Our search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb-1, with 4.9 fb-1 at 7 TeV and 19.7 fb-1 at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSM parameter space for different benchmark scenarios, m h max , m h mod + , m hmod - , light-stop, light-stau, τ-phobic, and low-m H. Lastly, upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given.

  3. Search for neutral MSSM Higgs bosons decaying to a pair of tau leptons in pp collisions

    DOE PAGESBeta

    Khachatryan, Vardan

    2014-10-28

    Our search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb-1, with 4.9 fb-1 at 7 TeV and 19.7 fb-1 at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSMmore » parameter space for different benchmark scenarios, m h max , m h mod + , m hmod - , light-stop, light-stau, τ-phobic, and low-m H. Lastly, upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given.« less

  4. Search for neutral MSSM Higgs bosons decaying to a pair of tau leptons in pp collisions

    NASA Astrophysics Data System (ADS)

    Khachatryan, V.; Sirunyan, A. M.; Tumasyan, A.; Adam, W.; Bergauer, T.; Dragicevic, M.; Er, J.; Fabjan, C.; Friedl, M.; Frhwirth, R.; Ghete, V. M.; Hartl, C.; Hrmann, N.; Hrubec, J.; Jeitler, M.; Kiesenhofer, W.; Knnz, V.; Krammer, M.; Krtschmer, I.; Liko, D.; Mikulec, I.; Rabady, D.; Rahbaran, B.; Rohringer, H.; Schfbeck, R.; Strauss, J.; Taurok, A.; Treberer-Treberspurg, W.; Waltenberger, W.; Wulz, C.-E.; Mossolov, V.; Shumeiko, N.; Suarez Gonzalez, J.; Alderweireldt, S.; Bansal, M.; Bansal, S.; Cornelis, T.; De Wolf, E. A.; Janssen, X.; Knutsson, A.; Luyckx, S.; Ochesanu, S.; Rougny, R.; Van De Klundert, M.; Van Haevermaet, H.; Van Mechelen, P.; Van Remortel, N.; Van Spilbeeck, A.; Blekman, F.; Blyweert, S.; D'Hondt, J.; Daci, N.; Heracleous, N.; Keaveney, J.; Lowette, S.; Maes, M.; Olbrechts, A.; Python, Q.; Strom, D.; Tavernier, S.; Van Doninck, W.; Van Mulders, P.; Van Onsem, G. P.; Villella, I.; Caillol, C.; Clerbaux, B.; De Lentdecker, G.; Dobur, D.; Favart, L.; Gay, A. P. R.; Grebenyuk, A.; Lonard, A.; Mohammadi, A.; Perni, L.; Reis, T.; Seva, T.; Thomas, L.; Vander Velde, C.; Vanlaer, P.; Wang, J.; Zenoni, F.; Adler, V.; Beernaert, K.; Benucci, L.; Cimmino, A.; Costantini, S.; Crucy, S.; Dildick, S.; Fagot, A.; Garcia, G.; Mccartin, J.; Ocampo Rios, A. A.; Ryckbosch, D.; Salva Diblen, S.; Sigamani, M.; Strobbe, N.; Thyssen, F.; Tytgat, M.; Yazgan, E.; Zaganidis, N.; Basegmez, S.; Beluffi, C.; Bruno, G.; Castello, R.; Caudron, A.; Ceard, L.; Da Silveira, G. G.; Delaere, C.; du Pree, T.; Favart, D.; Forthomme, L.; Giammanco, A.; Hollar, J.; Jafari, A.; Jez, P.; Komm, M.; Lemaitre, V.; Nuttens, C.; Pagano, D.; Perrini, L.; Pin, A.; Piotrzkowski, K.; Popov, A.; Quertenmont, L.; Selvaggi, M.; Vidal Marono, M.; Vizan Garcia, J. M.; Beliy, N.; Caebergs, T.; Daubie, E.; Hammad, G. H.; Ald, W. L.; Alves, G. A.; Brito, L.; Correa Martins, M.; Dos Reis Martins, T.; Mora Herrera, C.; Pol, M. E.; Carvalho, W.; Chinellato, J.; Custdio, A.; Da Costa, E. M.; De Jesus Damiao, D.; De Oliveira Martins, C.; Fonseca De Souza, S.; Malbouisson, H.; Matos Figueiredo, D.; Mundim, L.; Nogima, H.; Prado Da Silva, W. L.; Santaolalla, J.; Santoro, A.; Sznajder, A.; Tonelli Manganote, E. J.; Vilela Pereira, A.; Bernardes, C. A.; Dogra, S.; Fernandez Perez Tomei, T. R.; Gregores, E. M.; Mercadante, P. G.; Novaes, S. F.; Padula, Sandra S.; Aleksandrov, A.; Genchev, V.; Iaydjiev, P.; Marinov, A.; Piperov, S.; Rodozov, M.; Stoykova, S.; Sultanov, G.; Tcholakov, V.; Vutova, M.; Dimitrov, A.; Glushkov, I.; Hadjiiska, R.; Kozhuharov, V.; Litov, L.; Pavlov, B.; Petkov, P.; Bian, J. G.; Chen, G. M.; Chen, H. S.; Chen, M.; Du, R.; Jiang, C. H.; Plestina, R.; Tao, J.; Wang, Z.; Asawatangtrakuldee, C.; Ban, Y.; Li, Q.; Liu, S.; Mao, Y.; Qian, S. J.; Wang, D.; Zou, W.; Avila, C.; Chaparro Sierra, L. F.; Florez, C.; Gomez, J. P.; Gomez Moreno, B.; Sanabria, J. C.; Godinovic, N.; Lelas, D.; Polic, D.; Puljak, I.; Antunovic, Z.; Kovac, M.; Brigljevic, V.; Kadija, K.; Luetic, J.; Mekterovic, D.; Sudic, L.; Attikis, A.; Mavromanolakis, G.; Mousa, J.; Nicolaou, C.; Ptochos, F.; Razis, P. A.; Bodlak, M.; Finger, M.; Finger, M.; Assran, Y.; Ellithi Kamel, A.; Mahmoud, M. A.; Radi, A.; Kadastik, M.; Murumaa, M.; Raidal, M.; Tiko, A.; Eerola, P.; Fedi, G.; Voutilainen, M.; Hrknen, J.; Karimki, V.; Kinnunen, R.; Kortelainen, M. J.; Lampn, T.; Lassila-Perini, K.; Lehti, S.; Lindn, T.; Luukka, P.; Menp, T.; Peltola, T.; Tuominen, E.; Tuominiemi, J.; Tuovinen, E.; Wendland, L.; Talvitie, J.; Tuuva, T.; Besancon, M.; Couderc, F.; Dejardin, M.; Denegri, D.; Fabbro, B.; Faure, J. L.; Favaro, C.; Ferri, F.; Ganjour, S.; Givernaud, A.; Gras, P.; Hamel de Monchenault, G.; Jarry, P.; Locci, E.; Malcles, J.; Rander, J.; Rosowsky, A.; Titov, M.; Baffioni, S.; Beaudette, F.; Busson, P.; Charlot, C.; Dahms, T.; Dalchenko, M.; Dobrzynski, L.; Filipovic, N.; Florent, A.; Granier de Cassagnac, R.; Mastrolorenzo, L.; Min, P.; Mironov, C.; Naranjo, I. N.; Nguyen, M.; Ochando, C.; Paganini, P.; Regnard, S.; Salerno, R.; Sauvan, J. B.; Sirois, Y.; Veelken, C.; Yilmaz, Y.; Zabi, A.; Agram, J.-L.; Andrea, J.; Aubin, A.; Bloch, D.; Brom, J.-M.; Chabert, E. C.; Collard, C.; Conte, E.; Fontaine, J.-C.; Gel, D.; Goerlach, U.; Goetzmann, C.; Le Bihan, A.-C.; Van Hove, P.; Gadrat, S.; Beauceron, S.; Beaupere, N.; Boudoul, G.; Bouvier, E.; Brochet, S.; Carrillo Montoya, C. A.; Chasserat, J.; Chierici, R.; Contardo, D.; Depasse, P.; El Mamouni, H.; Fan, J.; Fay, J.; Gascon, S.; Gouzevitch, M.; Ille, B.; Kurca, T.; Lethuillier, M.; Mirabito, L.; Perries, S.; Ruiz Alvarez, J. D.; Sabes, D.; Sgandurra, L.; Sordini, V.; Vander Donckt, M.; Verdier, P.; Viret, S.; Xiao, H.; Tsamalaidze, Z.; Autermann, C.; Beranek, S.

    2014-10-01

    A search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb-1, with 4.9 fb-1 at 7 TeV and 19.7 fb-1 at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSM parameter space for different benchmark scenarios, m {h/max}, m {h/mod +}, m {h/mod -}, light-stop, light-stau, ?-phobic, and low- m H. Upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given. [Figure not available: see fulltext.

  5. Search for neutral MSSM Higgs bosons decaying to a pair of tau leptons in pp collisions

    DOE PAGESBeta

    Khachatryan, V.

    2014-10-28

    A search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb?, with 4.9 fb? at 7 TeV and 19.7 fb? at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSMmoreparameter space for different benchmark scenarios, mhmax, mhmod+ , mhmod , light-stop, light-stau, ?-phobic, and low-mH. Upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given.less

  6. Search for neutral MSSM Higgs bosons decaying to a pair of tau leptons in pp collisions

    SciTech Connect

    Khachatryan, V.

    2014-10-28

    A search for neutral Higgs bosons in the minimal supersymmetric extension of the standard model (MSSM) decaying to tau-lepton pairs in pp collisions is performed, using events recorded by the CMS experiment at the LHC. The dataset corresponds to an integrated luminosity of 24.6 fb?, with 4.9 fb? at 7 TeV and 19.7 fb? at 8 TeV. To enhance the sensitivity to neutral MSSM Higgs bosons, the search includes the case where the Higgs boson is produced in association with a b-quark jet. No excess is observed in the tau-lepton-pair invariant mass spectrum. Exclusion limits are presented in the MSSM parameter space for different benchmark scenarios, mhmax, mhmod+ , mhmod , light-stop, light-stau, ?-phobic, and low-mH. Upper limits on the cross section times branching fraction for gluon fusion and b-quark associated Higgs boson production are also given.

  7. Hyperphosphorylation-Induced Tau Oligomers

    PubMed Central

    Iqbal, Khalid; Gong, Cheng-Xin; Liu, Fei

    2013-01-01

    In normal adult brain the microtubule associated protein (MAP) tau contains 23 phosphates per mol of the protein and at this level of phosphorylation it is a soluble cytosolic protein. The normal brain tau interacts with tubulin and promotes its assembly into microtubules and stabilizes these fibrils. In Alzheimer disease (AD) brain tau is three to fourfold hyperphosphorylated. The abnormally hyperphosphorylated tau binds to normal tau instead of the tubulin and this binding leads to the formation of tau oligomers. The tau oligomers can be sedimented at 200,000??g whereas the normal tau under these conditions remains in the supernatant. The abnormally hyperphosphorylated tau is capable of sequestering not only normal tau but also MAP MAP1 and MAP2 and causing disruption of the microtubule network promoted by these proteins. Unlike A? and prion protein (PrP) oligomers, tau oligomerization in AD and related tauopathies is hyperphosphorylation-dependent; in vitro dephosphorylation of AD P-tau with protein phosphatase 2A (PP2A) inhibits and rehyperphosphorylation of the PP2A-AD P-tau with more than one combination of tau protein kinases promotes its oligomerization. In physiological assembly conditions the AD P-tau readily self-assembles into paired helical filaments. Missense tau mutations found in frontotemporal dementia apparently lead to tau oligomerization and neurofibrillary pathology by promoting its abnormal hyperphosphorylation. Dysregulation of the alternative splicing of tau that alters the 1:1 ratio of the 3-repeat: 4-repeat taus such as in Down syndrome, Pick disease, and progressive supranuclear palsy leads to the abnormal hyperphosphorylation of tau. PMID:23966973

  8. The Search for B+ to Tau+ Nu(Tau) at BaBar

    SciTech Connect

    Corwin, L.A.; /SLAC

    2007-01-08

    We present a search for the decay B{sup +} {yields} {tau}{sup +}{nu}{sub {tau}} using 288 fb{sup -1} of data collected at the {Upsilon}(4S) resonance with the BABAR detector at the SLAC PEP-II B-Factory. A sample of events with one reconstructed semileptonic B decay (B{sup -} {yields} D{sup o}{ell}{sup -}{bar {nu}}{sub {ell}}X) is selected, and in the recoil a search for B{sup +} {yields} {tau}{sup +}{nu}{sub {tau}} signal is performed. The {tau} is identified in the following channels: {tau}{sup +} {yields} e{sup +}{nu}{sub e}{bar {nu}}{sub {tau}}, {tau}{sup +} {yields} {mu}{sup +} {nu}{sub {mu}}{bar {nu}}{sub {tau}}, {tau}{sup +} {yields} {pi}{sup +}{pi}{sup 0}{bar {nu}}{sub {tau}}. We measure a branching fraction of {Beta}(B{sup +} {yields} {tau}{sup +}{nu}{sub {tau}}) = 0.88{sub -0.67}{sup +0.68}(stat.) {+-} 0.11(syst.) x 10{sup -4} and extract an upper limit on the branching fraction, at the 90% confidence level, of {Beta}(B{sup +} {yields} {tau}{sup +}{nu}{sub {tau}}) < 1.8 x 10{sup -4}. We calculate the product of the B meson decay constant and |V{sub ub}| to be f{sub B} {center_dot} |V{sub ub}| = (7.0{sub -3.6}{sup +2.3}(stat.){sub -0.5}{sup +0.4}(syst.)) x 10{sup -4} GeV.

  9. Search for Charged Higgs Boson Decays of the Top Quark using Hadronic Decays of the Tau Lepton

    NASA Astrophysics Data System (ADS)

    Abe, F.; Akimoto, H.; Akopian, A.; Albrow, M. G.; Amendolia, S. R.; Amidei, D.; Antos, J.; Aota, S.; Apollinari, G.; Asakawa, T.; Ashmanskas, W.; Atac, M.; Azfar, F.; Azzi-Bacchetta, P.; Bacchetta, N.; Badgett, W.; Bagdasarov, S.; Bailey, M. W.; Bao, J.; de Barbaro, P.; Barbaro-Galtieri, A.; Barnes, V. E.; Barnett, B. A.; Barone, M.; Barzi, E.; Bauer, G.; Baumann, T.; Bedeschi, F.; Behrends, S.; Belforte, S.; Bellettini, G.; Bellinger, J.; Benjamin, D.; Benlloch, J.; Bensinger, J.; Benton, D.; Beretvas, A.; Berge, J. P.; Berryhill, J.; Bertolucci, S.; Bevensee, B.; Bhatti, A.; Biery, K.; Binkley, M.; Bisello, D.; Blair, R. E.; Blocker, C.; Bodek, A.; Bokhari, W.; Bolognesi, V.; Bolla, G.; Bortoletto, D.; Boudreau, J.; Breccia, L.; Bromberg, C.; Bruner, N.; Buckley-Geer, E.; Budd, H. S.; Burkett, K.; Busetto, G.; Byon-Wagner, A.; Byrum, K. L.; Cammerata, J.; Campagnari, C.; Campbell, M.; Caner, A.; Carithers, W.; Carlsmith, D.; Castro, A.; Cauz, D.; Cen, Y.; Cervelli, F.; Chang, P. S.; Chang, P. T.; Chao, H. Y.; Chapman, J.; Cheng, M.-T.; Chiarelli, G.; Chikamatsu, T.; Chiou, C. N.; Christofek, L.; Cihangir, S.; Clark, A. G.; Cobal, M.; Cocca, E.; Contreras, M.; Conway, J.; Cooper, J.; Cordelli, M.; Couyoumtzelis, C.; Crane, D.; Cronin-Hennessy, D.; Culbertson, R.; Daniels, T.; Dejongh, F.; Delchamps, S.; dell'Agnello, S.; dell'Orso, M.; Demina, R.; Demortier, L.; Deninno, M.; Derwent, P. F.; Devlin, T.; Dittmann, J. R.; Donati, S.; Done, J.; Dorigo, T.; Dunn, A.; Eddy, N.; Einsweiler, K.; Elias, J. E.; Ely, R.; Engels, E., Jr.; Errede, D.; Errede, S.; Fan, Q.; Feild, G.; Ferretti, C.; Fiori, I.; Flaugher, B.; Foster, G. W.; Franklin, M.; Frautschi, M.; Freeman, J.; Friedman, J.; Frisch, H.; Fukui, Y.; Funaki, S.; Galeotti, S.; Gallinaro, M.; Ganel, O.; Garcia-Sciveres, M.; Garfinkel, A. F.; Gay, C.; Geer, S.; Gerdes, D. W.; Giannetti, P.; Giokaris, N.; Giromini, P.; Giusti, G.; Gladney, L.; Glenzinski, D.; Gold, M.; Gonzalez, J.; Gordon, A.; Goshaw, A. T.; Gotra, Y.; Goulianos, K.; Grassmann, H.; Groer, L.; Grosso-Pilcher, C.; Guillian, G.; Guo, R. S.; Haber, C.; Hafen, E.; Hahn, S. R.; Hamilton, R.; Handler, R.; Hans, R. M.; Happacher, F.; Hara, K.; Hardman, A. D.; Harral, B.; Harris, R. M.; Hauger, S. A.; Hauser, J.; Hawk, C.; Hayashi, E.; Heinrich, J.; Hinrichsen, B.; Hoffman, K. D.; Hohlmann, M.; Holck, C.; Hollebeek, R.; Holloway, L.; Hong, S.; Houk, G.; Hu, P.; Huffman, B. T.; Hughes, R.; Huston, J.; Huth, J.; Hylen, J.; Ikeda, H.; Incagli, M.; Incandela, J.; Introzzi, G.; Iwai, J.; Iwata, Y.; Jensen, H.; Joshi, U.; Kadel, R. W.; Kajfasz, E.; Kambara, H.; Kamon, T.; Kaneko, T.; Karr, K.; Kasha, H.; Kato, Y.; Keaffaber, T. A.; Kelley, K.; Kennedy, R. D.; Kephart, R.; Kesten, P.; Kestenbaum, D.; Keutelian, H.; Keyvan, F.; Kharadia, B.; Kim, B. J.; Kim, D. H.; Kim, H. S.; Kim, S. B.; Kim, S. H.; Kim, Y. K.; Kirsch, L.; Koehn, P.; Kondo, K.; Konigsberg, J.; Kopp, S.; Kordas, K.; Korytov, A.; Koska, W.; Kovacs, E.; Kowald, W.; Krasberg, M.; Kroll, J.; Kruse, M.; Kuwabara, T.; Kuhlmann, S. E.; Kuns, E.; Laasanen, A. T.; Lami, S.; Lammel, S.; Lamoureux, J. I.; Lancaster, M.; Lecompte, T.; Leone, S.; Lewis, J. D.; Limon, P.; Lindgren, M.; Liss, T. M.; Liu, J. B.; Liu, Y. C.; Lockyer, N.; Long, O.; Loomis, C.; Loreti, M.; Lu, J.; Lucchesi, D.; Lukens, P.; Lusin, S.; Lys, J.; Maeshima, K.; Maghakian, A.; Maksimovic, P.; Mangano, M.; Mansour, J.; Mariotti, M.; Marriner, J. P.; Martin, A.; Matthews, J. A.; Mattingly, R.; McIntyre, P.; Melese, P.; Menzione, A.; Meschi, E.; Metzler, S.; Miao, C.; Miao, T.; Michail, G.; Miller, R.; Minato, H.; Miscetti, S.; Mishina, M.; Mitsushio, H.; Miyamoto, T.; Miyashita, S.; Moggi, N.; Morita, Y.; Mukherjee, A.; Muller, T.; Murat, P.; Nakada, H.; Nakano, I.; Nelson, C.; Neuberger, D.; Newman-Holmes, C.; Ngan, C.-Y. P.; Ninomiya, M.; Nodulman, L.; Oh, S. H.; Ohl, K. E.; Ohmoto, T.; Ohsugi, T.; Oishi, R.; Okabe, M.; Okusawa, T.; Oliveira, R.; Olsen, J.; Pagliarone, C.; Paoletti, R.; Papadimitriou, V.; Pappas, S. P.; Parashar, N.; Park, S.; Parri, A.; Patrick, J.; Pauletta, G.; Paulini, M.; Perazzo, A.; Pescara, L.; Peters, M. D.; Phillips, T. J.; Piacentino, G.; Pillai, M.; Pitts, K. T.; Plunkett, R.; Pondrom, L.; Proudfoot, J.; Ptohos, F.; Punzi, G.; Ragan, K.; Reher, D.; Ribon, A.; Rimondi, F.; Ristori, L.; Robertson, W. J.; Rodrigo, T.; Rolli, S.; Romano, J.; Rosenson, L.; Roser, R.; Saab, T.; Sakumoto, W. K.; Saltzberg, D.; Sansoni, A.; Santi, L.; Sato, H.; Schlabach, P.; Schmidt, E. E.; Schmidt, M. P.; Scribano, A.; Segler, S.; Seidel, S.; Seiya, Y.; Sganos, G.; Shapiro, M. D.; Shaw, N. M.; Shen, Q.; Shepard, P. F.; Shimojima, M.; Shochet, M.; Siegrist, J.; Sill, A.; Sinervo, P.; Singh, P.; Skarha, J.; Sliwa, K.; Snider, F. D.; Song, T.; Spalding, J.; Speer, T.; Sphicas, P.; Spinella, F.; Spiropulu, M.

    1997-07-01

    This Letter describes a direct search for charged Higgs boson production in pp collisions at s = 1.8 TeV recorded by the Collider Detector at Fermilab. Two-Higgs-double extensions to the standard model predict the existence of charged Higgs bosons \\(H+/-\\). In such models, the branching fraction for top quarks B\\(t-->H+b-->?+?b\\) can be large. This search uses the hadronic decays of the tau lepton in this channel to significantly extend previous limits on H+/- production.

  10. Charged particle pair production associated with a lepton pair in Z decays. indication of an excess in the tau channel

    NASA Astrophysics Data System (ADS)

    Decamp, D.; Deschizeaux, B.; Goy, C.; Lees, J.-P.; Minard, M.-N.; Alemany, R.; Crespo, J. M.; Delfino, M.; Fernandez, E.; Gaitan, V.; Garrido, Ll.; Mir, Ll. M.; Pacheco, A.; Catanesi, M. G.; Creanza, D.; de Palma, M.; Farilla, A.; Iaselli, G.; Maggi, G.; Maggi, M.; Natali, S.; Nuzzo, S.; Quattromini, M.; Ranieri, A.; Raso, G.; Romano, F.; Ruggieri, F.; Selvaggi, G.; Silvestris, L.; Tempesta, P.; Zito, G.; Gao, Y.; Hu, H.; Huang, D.; Huang, X.; Lin, J.; Lou, J.; Qiao, C.; Ruan, T.; Wang, T.; Xie, Y.; Xu, D.; Xu, R.; Zhang, J.; Zhao, W.; Atwood, W. B.; Bauerdick, L. A. T.; Bird, F.; Blucher, E.; Bonvicini, G.; Bossi, F.; Brown, D.; Burnett, T. H.; Drevermann, H.; Forty, R. W.; Grab, C.; Hagelberg, R.; Haywood, S.; Hilgart, J.; Jost, B.; Kasemann, M.; Knobloch, J.; Lacourt, A.; Lanon, E.; Lehraus, I.; Lohse, T.; Marchioro, A.; Martinez, M.; Mato, P.; Menary, S.; Minten, A.; Miotto, A.; Miquel, R.; Moser, H.-G.; Nash, J.; Palazzi, P.; Ranjard, F.; Redlinger, G.; Roth, A.; Rothberg, J.; Rotscheidt, H.; St. Denis, R.; Schlatter, D.; Takashima, M.; Talby, M.; Tejessy, W.; Wachsmuth, H.; Wasserbaech, S.; Wheeler, S.; Wiedenmann, W.; Witzeling, W.; Wotschack, J.; Wu, W.; Ajaltouni, Z.; Bardadin-Otwinowska, M.; Falvard, A.; El Fellous, R.; Gay, P.; Harvey, J.; Henrard, P.; Jousset, J.; Michel, B.; Montret, J.-C.; Pallin, D.; Perret, P.; Proriol, J.; Prulhire, F.; Stimpfl, G.; Hansen, J. D.; Hansen, J. R.; Hansen, P. H.; Mllerud, R.; Nielsen, E. R.; Nilsson, B. S.; Efthymiopoulos, I.; Simopoulou, E.; Vayaki, A.; Badier, J.; Blondel, A.; Bonneaud, G.; Bourotte, J.; Braems, F.; Brient, J. C.; Fouque, G.; Gamess, A.; Guirlet, R.; Orteu, S.; Rosowsky, A.; Roug, A.; Rumpf, M.; Tanaka, R.; Videau, H.; Candlin, D. J.; Veitch, E.; Parrini, G.; Corden, M.; Georgiopoulos, C.; Ikeda, M.; Lannutti, J.; Levinthal, D.; Mermikides, M.; Sawyer, L.; Antonelli, A.; Baldini, R.; Bencivenni, G.; Bologna, G.; Campana, P.; Capon, G.; Cerutti, F.; Chiarella, V.; D'Ettorre-Piazzoli, B.; Felici, G.; Laurelli, P.; Mannocchi, G.; Murtas, F.; Murtas, G. P.; Nicoletti, G.; Passalacqua, L.; Pepe-Altarelli, M.; Picchi, P.; Zografou, P.; Altoon, B.; Boyle, O.; Halley, A. W.; Ten Have, I.; Hearns, J. L.; Lynch, J. G.; Morton, W. T.; Raine, C.; Scarr, J. M.; Smith, K.; Thompson, A. S.; Turnbull, R. M.; Brandl, B.; Braun, O.; Geiges, R.; Geweniger, C.; Hanke, P.; Hepp, V.; Kluge, E. E.; Maumary, Y.; Putzer, A.; Rensch, B.; Stahl, A.; Tittel, K.; Wunsch, M.; Belk, A. T.; Beuselinck, R.; Binnie, D. M.; Cameron, W.; Cattaneo, M.; Dornan, P. J.; Dugeay, S.; Greene, A. M.; Lieske, N. M.; Patton, S. J.; Payne, D. G.; Phillips, M. J.; Sedgbeer, J. K.; Taylor, G.; Tomalin, I. R.; Wright, A. G.; Girtler, P.; Kuhn, D.; Rudolph, G.; Bowdery, C. K.; Brodbeck, T. J.; Finch, A. J.; Foster, F.; Hughes, G.; Keemer, N. R.; Nuttall, M.; Patel, A.; Rowlingson, B. S.; Sloan, T.; Snow, S. W.; Whelan, E. P.; Barczewski, T.; Kleinknecht, K.; Raab, J.; Renk, B.; Roehn, S.; Sander, H.-G.; Schmelling, M.; Schmidt, H.; Steeg, F.; Walther, S. M.; Wolf, B.; Albanese, J.-P.; Aubert, J.-J.; Benchouk, C.; Bernard, V.; Bonissent, A.; Courvoisier, D.; Etienne, F.; Papalexiou, S.; Payre, P.; Pietrzyk, B.; Qian, Z.; Becker, H.; Blum, W.; Cattaneo, P.; Cowan, G.; Dehning, B.; Dietl, H.; Dydak, F.; Fernandez-Bosman, M.; Hansl-Kozanecka, T.; Jahn, A.; Kozanecki, W.; Lange, E.; Lauber, J.; Ltjens, G.; Lutz, G.; Mnner, W.; Pan, Y.; Richter, R.; Schrder, J.; Schwarz, A. S.; Settles, R.; Stierlin, U.; Thomas, J.; Wolf, G.; Bertin, V.; Boucrot, J.; Callot, O.; Chen, X.; Cordier, A.; Ganis, M.; Grivaz, J.-F.; Heusse, Ph.; Janot, P.; Kim, D. W.; Le Diberder, F.; Lefranois, J.; Lutz, A.-M.; Veillet, J.-J.; Videau, I.; Zhang, Z.; Zomer, F.; Abbaneo, D.; Amendolia, S. R.; Bagliesi, G.; Batignani, G.; Bosisio, L.; Bottigli, U.; Bradaschia, C.; Carpinelli, M.; Ciocci, M. A.; Dell'Orso, R.; Ferrante, I.; Fidecaro, F.; Fo, L.; Focardi, E.; Forti, F.; Giassi, A.; Giorgi, M. A.; Ligabue, F.; Lusiani, A.; Mannelli, E. B.; Marrocchesi, P. S.; Messineo, A.; Moneta, L.; Palla, F.; Sanguinetti, G.; Steinberger, J.; Tenchini, R.; Tonelli, G.; Triggiani, G.; Vannini, C.; Venturi, A.; Verdini, P. G.; Walsh, J.; Carter, J. M.; Green, M. G.; March, P. V.; Medcalf, T.; Quazi, I. S.; Saich, M. R.; Strong, J. A.; Thomas, R. M.; West, L. R.; Wildish, T.; Botterill, D. R.; Clifft, R. W.; Edgecock, T. R.; Edwards, M.; Fisher, S. M.; Jones, T. J.; Norton, P. R.; Salmon, D. P.; Thompson, J. C.; Bloch-Devaux, B.; Colas, P.; Klopfenstein, C.; Locci, E.; Loucatos, S.; Monnier, E.; Perez, P.; Perlas, J. A.; Perrier, F.; Rander, J.; Renardy, J.-F.; Roussarie, A.; Schuller, J.-P.; Schwindling, J.; Vallage, B.; Ashman, J. G.; Booth, C. N.; Buttar, C.; Carney, R.; Cartwright, S.; Combley, F.; Dinsdale, M.; Dogru, M.

    1991-07-01

    In a sample of 200 000 Z decays, events with two leptons and an additional pair of charged particles are studied. The 35 events found show a possible excess in the tau channel compared with the expectation from electroweak processes. The features of the events are consistent with radiation of virtual photons.

  11. Search for Higgs bosons decaying to tau pairs in pp over collisions with the D0 detector.

    PubMed

    Abazov, V M; Abbott, B; Abolins, M; Acharya, B S; Adams, M; Adams, T; Aguilo, E; Ahn, S H; Ahsan, M; Alexeev, G D; Alkhazov, G; Alton, A; Alverson, G; Alves, G A; Anastasoaie, M; Ancu, L S; Andeen, T; Anderson, S; Andrieu, B; Anzelc, M S; Aoki, M; Arnoud, Y; Arov, M; Arthaud, M; Askew, A; Asman, B; Assis Jesus, A C S; Atramentov, O; Avila, C; Badaud, F; Baden, A; Bagby, L; Baldin, B; Bandurin, D V; Banerjee, P; Banerjee, S; Barberis, E; Barfuss, A-F; Bargassa, P; Baringer, P; Barreto, J; Bartlett, J F; Bassler, U; Bauer, D; Beale, S; Bean, A; Begalli, M; Begel, M; Belanger-Champagne, C; Bellantoni, L; Bellavance, A; Benitez, J A; Beri, S B; Bernardi, G; Bernhard, R; Bertram, I; Besançon, M; Beuselinck, R; Bezzubov, V A; Bhat, P C; Bhatnagar, V; Biscarat, C; Blazey, G; Blekman, F; Blessing, S; Bloch, D; Bloom, K; Boehnlein, A; Boline, D; Bolton, T A; Boos, E E; Borissov, G; Bose, T; Brandt, A; Brock, R; Brooijmans, G; Bross, A; Brown, D; Buchanan, N J; Buchholz, D; Buehler, M; Buescher, V; Bunichev, V; Burdin, S; Burke, S; Burnett, T H; Buszello, C P; Butler, J M; Calfayan, P; Calvet, S; Cammin, J; Carvalho, W; Casey, B C K; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K; Chan, K M; Chandra, A; Charles, F; Cheu, E; Chevallier, F; Cho, D K; Choi, S; Choudhary, B; Christofek, L; Christoudias, T; Cihangir, S; Claes, D; Clutter, J; Cooke, M; Cooper, W E; Corcoran, M; Couderc, F; Cousinou, M-C; Crépé-Renaudin, S; Cutts, D; Cwiok, M; da Motta, H; Das, A; Davies, G; De, K; de Jong, S J; De La Cruz-Burelo, E; De Oliveira Martins, C; Degenhardt, J D; Déliot, F; Demarteau, M; Demina, R; Denisov, D; Denisov, S P; Desai, S; Diehl, H T; Diesburg, M; Dominguez, A; Dong, H; Dudko, L V; Duflot, L; Dugad, S R; Duggan, D; Duperrin, A; Dyer, J; Dyshkant, A; Eads, M; Edmunds, D; Ellison, J; Elvira, V D; Enari, Y; Eno, S; Ermolov, P; Evans, H; Evdokimov, A; Evdokimov, V N; Ferapontov, A V; Ferbel, T; Fiedler, F; Filthaut, F; Fisher, W; Fisk, H E; Fortner, M; Fox, H; Fu, S; Fuess, S; Gadfort, T; Galea, C F; Gallas, E; Garcia, C; Garcia-Bellido, A; Gavrilov, V; Gay, P; Geist, W; Gelé, D; Gerber, C E; Gershtein, Y; Gillberg, D; Ginther, G; Gollub, N; Gómez, B; Goussiou, A; Grannis, P D; Greenlee, H; Greenwood, Z D; Gregores, E M; Grenier, G; Gris, Ph; Grivaz, J-F; Grohsjean, A; Grünendahl, S; Grünewald, M W; Guo, F; Guo, J; Gutierrez, G; Gutierrez, P; Haas, A; Hadley, N J; Haefner, P; Hagopian, S; Haley, J; Hall, I; Hall, R E; Han, L; Harder, K; Harel, A; Hauptman, J M; Hauser, R; Hays, J; Hebbeker, T; Hedin, D; Hegeman, J G; Heinson, A P; Heintz, U; Hensel, C; Herner, K; Hesketh, G; Hildreth, M D; Hirosky, R; Hobbs, J D; Hoeneisen, B; Hoeth, H; Hohlfeld, M; Hong, S J; Hossain, S; Houben, P; Hu, Y; Hubacek, Z; Hynek, V; Iashvili, I; Illingworth, R; Ito, A S; Jabeen, S; Jaffré, M; Jain, S; Jakobs, K; Jarvis, C; Jesik, R; Johns, K; Johnson, C; Johnson, M; Jonckheere, A; Jonsson, P; Juste, A; Kajfasz, E; Kalk, J M; Karmanov, D; Kasper, P A; Katsanos, I; Kau, D; Kaushik, V; Kehoe, R; Kermiche, S; Khalatyan, N; Khanov, A; Kharchilava, A; Kharzheev, Y M; Khatidze, D; Kim, T J; Kirby, M H; Kirsch, M; Klima, B; Kohli, J M; Konrath, J-P; Kozelov, A V; Kraus, J; Krop, D; Kuhl, T; Kumar, A; Kupco, A; Kurca, T; Kuzmin, V A; Kvita, J; Lacroix, F; Lam, D; Lammers, S; Landsberg, G; Lebrun, P; Lee, W M; Leflat, A; Lellouch, J; Leveque, J; Li, J; Li, L; Li, Q Z; Lietti, S M; Lima, J G R; Lincoln, D; Linnemann, J; Lipaev, V V; Lipton, R; Liu, Y; Liu, Z; Lobodenko, A; Lokajicek, M; Love, P; Lubatti, H J; Luna, R; Lyon, A L; Maciel, A K A; Mackin, D; Madaras, R J; Mättig, P; Magass, C; Magerkurth, A; Mal, P K; Malbouisson, H B; Malik, S; Malyshev, V L; Mao, H S; Maravin, Y; Martin, B; McCarthy, R; Melnitchouk, A; Mendoza, L; Mercadante, P G; Merkin, M; Merritt, K W; Meyer, A; Meyer, J; Millet, T; Mitrevski, J; Mommsen, R K; Mondal, N K; Moore, R W; Moulik, T; Muanza, G S; Mulhearn, M; Mundal, O; Mundim, L; Nagy, E; Naimuddin, M; Narain, M; Naumann, N A; Neal, H A; Negret, J P; Neustroev, P; Nilsen, H; Nogima, H; Novaes, S F; Nunnemann, T; O'Dell, V; O'Neil, D C; Obrant, G; Ochando, C; Onoprienko, D; Oshima, N; Osman, N; Osta, J; Otec, R; Otero y Garzón, G J; Owen, M; Padley, P; Pangilinan, M; Parashar, N; Park, S-J; Park, S K; Parsons, J; Partridge, R; Parua, N; Patwa, A; Pawloski, G; Penning, B; Perfilov, M; Peters, K; Peters, Y; Pétroff, P; Petteni, M; Piegaia, R; Piper, J; Pleier, M-A; Podesta-Lerma, P L M; Podstavkov, V M; Pogorelov, Y; Pol, M-E; Polozov, P; Pope, B G; Popov, A V; Potter, C; da Silva, W L Prado; Prosper, H B; Protopopescu, S; Qian, J; Quadt, A; Quinn, B; Rakitine, A; Rangel, M S; Ranjan, K; Ratoff, P N; Renkel, P; Reucroft, S; Rich, P; Rieger, J; Rijssenbeek, M; Ripp-Baudot, I; Rizatdinova, F; Robinson, S; Rodrigues, R F; Rominsky, M; Royon, C; Rubinov, P; Ruchti, R; Safronov, G; Sajot, G; Sánchez-Hernández, A; Sanders, M P; Sanghi, B; Santoro, A; Savage, G; Sawyer, L; Scanlon, T; Schaile, D; Schamberger, R D; Scheglov, Y; Schellman, H; Schliephake, T; Schwanenberger, C; Schwartzman, A; Schwienhorst, R; Sekaric, J; Severini, H; Shabalina, E; Shamim, M; Shary, V; Shchukin, A A; Shivpuri, R K; Siccardi, V; Simak, V; Sirotenko, V; Skubic, P; Slattery, P; Smirnov, D; Snow, G R; Snow, J; Snyder, S; Söldner-Rembold, S; Sonnenschein, L; Sopczak, A; Sosebee, M; Soustruznik, K; Spurlock, B; Stark, J; Steele, J; Stolin, V; Stoyanova, D A; Strandberg, J; Strandberg, S; Strang, M A; Strauss, E; Strauss, M; Ströhmer, R; Strom, D; Stutte, L; Sumowidagdo, S; Svoisky, P; Sznajder, A; Tamburello, P; Tanasijczuk, A; Taylor, W; Temple, J; Tiller, B; Tissandier, F; Titov, M; Tokmenin, V V; Toole, T; Torchiani, I; Trefzger, T; Tsybychev, D; Tuchming, B; Tully, C; Tuts, P M; Unalan, R; Uvarov, L; Uvarov, S; Uzunyan, S; Vachon, B; van den Berg, P J; Van Kooten, R; van Leeuwen, W M; Varelas, N; Varnes, E W; Vasilyev, I A; Vaupel, M; Verdier, P; Vertogradov, L S; Verzocchi, M; Villeneuve-Seguier, F; Vint, P; Vokac, P; Von Toerne, E; Voutilainen, M; Wagner, R; Wahl, H D; Wang, L; Wang, M H L S; Warchol, J; Watts, G; Wayne, M; Weber, G; Weber, M; Welty-Rieger, L; Wenger, A; Wermes, N; Wetstein, M; White, A; Wicke, D; Wilson, G W; Wimpenny, S J; Wobisch, M; Wood, D R; Wyatt, T R; Xie, Y; Yacoob, S; Yamada, R; Yan, M; Yang, W-C; Yasuda, T; Yatsunenko, Y A; Yip, K; Yoo, H D; Youn, S W; Yu, J; Zeitnitz, C; Zhao, T; Zhou, B; Zhu, J; Zielinski, M; Zieminska, D; Zieminski, A; Zivkovic, L; Zutshi, V; Zverev, E G

    2008-08-15

    We present a search for the production of neutral Higgs bosons varphi decaying into tau+tau - final states in pp over collisions at a center-of-mass energy of 1.96 TeV. The data, corresponding to an integrated luminosity of approximately 1 fb(-1), were collected by the D0 experiment at the Fermilab Tevatron Collider. Limits on the production cross section times branching ratio are set. The results are interpreted in the minimal supersymmetric standard model yielding limits that are the most stringent to date at hadron colliders. PMID:18764524

  12. Implications of the ALEPH {tau} -Lepton Decay Data for Perturbative and Nonperturbative QCD

    SciTech Connect

    Scha''fer, Thomas; Shuryak, Edward V.

    2001-04-30

    We use ALEPH data on hadronic {tau} decays in order to calculate Euclidean coordinate space correlation functions in the vector and axial-vector channels. The linear combination V-A receives no perturbative contribution and is quantitatively reproduced by the instanton liquid model. In the case of V+A the instanton calculation is in good agreement with the data once perturbative corrections are included. These corrections clearly show the evolution of {alpha}{sub s} . We also analyze the range of validity of the operator product expansion (OPE). We conclude that the range of validity of the OPE is limited to x{approx}<0.3 fm , whereas the instanton model describes the data over the entire range.

  13. Tau appearance in atmospheric neutrino interactions

    SciTech Connect

    Hall, Lawrence J.; Murayama, Hitoshi

    1998-10-24

    If the correct interpretation of the Super-Kamiokande atmospheric neutrino data is {nu}{sub {mu}} {yields} {nu}{sub {tau}} oscillation, the contained data sample should already have more than 10 {tau} appearance events. We study the challenging task of detecting the {tau}, focusing on the decay chain {tau}{sup {+-}} {yields} {rho}{sup {+-}} {yields} {pi}{sup {+-}}{pi}{sup 0} in events with quasi-elastic {tau} production. The background level, which is currently quite uncertain because of a lack of relevant neutral current data, can be measured by the near detector in the K2K experiment. Our estimates of the background suggest that it may be possible to detect {tau} appearance in Super-Kamiokande with 5-10 years of running.

  14. Tau physics results from SLD

    SciTech Connect

    Daoudi, M.; SLD Collaboration

    1996-08-10

    Results on {tau} physics at SLD are presented. They are based on 4,316 {tau}-pair events selected from a 150 k Z{sup 0} data sample collected at the SLC. These results include measurements of the {tau} lifetime ({tau}{sub r} = 288.1 {+-} 6.1 {+-} 3.3 fs), the {tau} Michel parameters ({rho} = 0.71 {+-} 0.09 {+-} 0.04, {zeta} = 1.03 {+-} 0.36 {+-} 0.05, and {zeta}{delta} = 0.84 {+-} 0.27 {+-} 0.05), and the {tau} neutrino helicity (h{sub {nu}} = {minus}0.81 {+-} 0.18 {+-} 0.03).

  15. Zinc Binding Directly Regulates Tau Toxicity Independent of Tau Hyperphosphorylation

    PubMed Central

    Huang, Yunpeng; Wu, Zhihao; Cao, Yu; Lang, Minglin; Lu, Bingwei; Zhou, Bing

    2015-01-01

    SUMMARY Tau hyperphosphorylation is thought to underlie tauopathy. Working in a Drosophila tauopathy model expressing a human Tau mutant (hTauR406W, or Tau*), we show that zinc contributes to the development of Tau toxicity through two independent actions: by increasing Tau phosphorylation and, more significantly, by directly binding to Tau. Elimination of zinc binding through amino acid substitution of Cys residues has a minimal effect on phosphorylation levels yet essentially eliminates Tau toxicity. The toxicity of the zinc-binding-deficient mutant Tau* (Tau*C2A) and overexpression of native Drosophila Tau, also lacking the corresponding zinc-binding Cys residues, are largely impervious to zinc concentration. Importantly, restoration of zinc-binding ability to Tau* by introduction of a zinc-binding residue (His) into the original Cys positions restores zinc-responsive toxicities in proportion to zinc-binding affinities. These results indicate zinc binding is a substantial contributor to tauopathy and have implications for therapy development. PMID:25066125

  16. Review of recent results on the /tau/ lepton

    SciTech Connect

    Gan, K.K.

    1988-04-01

    This is a review of the recent results on the /tau/ lepton. The results include precise measurements of the lifetime, measurements of the decay /tau//sup /minus// ..-->.. ..pi../sup /minus//2..pi../sup 0/..nu../sub /tau// with much improved precision, limits on decay modes containing /eta/ mesons, including the second-class-current decay /tau//sup /minus// ..-->.. ..pi../sup /minus///eta/..nu../sub /tau//, and limits on exotic decay modes. The implications of these results on the discrepancy in the one-charged-particle decay modes are discussed. 43 refs., 4 figs., 2 tabs.

  17. Recent Results From BaBar in Tau Physics

    SciTech Connect

    Lewczuk, Mateusz; /Victoria U.

    2009-06-25

    The BaBar collaboration has accumulated over 400 million {tau}-pairs which can be used to study charged leptonic and hadronic weak currents to unprecedented precision. This note presents results on lepton universality, measurements of |V{sub us}|, and searches for {tau} decays which violate lepton flavour conservation, or {tau} decays that proceed through a suppressed second class current.

  18. Tau physics with polarized beams

    SciTech Connect

    Daoudi, M.

    1995-11-01

    We present the first results on tau physics using polarized beams. These include measurements of the {tau} Michel parameters {xi} and {xi}{delta} and the {tau} neutrino helicity h{sub {nu}}. The measurements were performed using the SLD detector at the Stanford Linear Collider (SLC).

  19. Impact of $\\tau$ polarization on the study of the MSSM charged Higgs bosons in top quark decays at the ILC

    SciTech Connect

    Boos, E.; Bunichev, V.; Carena, Marcela S.; Wagner, C.E.M.

    2005-07-01

    The process of top quark pair production at the ILC with subsequent decays of one of the top quarks to a charged Higgs boson and b-quark is considered. The charged Higgs decays to tau leptons whose polarization is the opposite to those coming from W bosons. This difference is reflected in the energy distributions of the tau decay products in the top quark rest frame, which can be reconstructed at the ILC using the recoil mass technique. We present an analysis including spin correlations, backgrounds, ISR/FSR and beamstrahlung, and show that a fit of the shape of the pion energy spectrum yields the charged Higgs boson mass with an accuracy of about 1 GeV.

  20. Potential synergy between tau aggregation inhibitors and tau chaperone modulators

    PubMed Central

    2013-01-01

    Tau is a soluble, microtubule-associated protein known to aberrantly form amyloid-positive aggregates. This pathology is characteristic for more than 15 neuropathies, the most common of which is Alzheimer’s disease. Finding therapeutics to reverse or remove this non-native tau state is of great interest; however, at this time only one drug is entering phase III clinical trials for treating tauopathies. Generally, tau manipulation by therapeutics can either directly or indirectly alter tau aggregation and stability. Drugs that bind and change the conformation of tau itself are largely classified as aggregation inhibitors, while drugs that alter the activity of a tau-effector protein fall into several categories, such as kinase inhibitors, microtubule stabilizers, or chaperone modulators. Chaperone inhibitors that have proven effective in tau models include heat shock protein 90 inhibitors, heat shock protein 70 inhibitors and activators, as well as inducers of heat shock proteins. While many of these compounds can alter tau levels and/or aggregation states, it is possible that combining these approaches may produce the most optimal outcome. However, because many of these compounds have multiple off-target effects or poor blood–brain barrier permeability, the development of this synergistic therapeutic strategy presents significant challenges. This review will summarize many of the drugs that have been identified to alter tau biology, with special focus on therapeutics that prevent tau aggregation and regulate chaperone-mediated clearance of tau. PMID:24041111

  1. Measurement of tau lepton branching fractions

    SciTech Connect

    Nicol, N.A.

    1993-09-30

    We present {tau}{sup {minus}} lepton branching fraction measurements based on data from the TPC/Two-Gamma detector at PEP. Using a sample of{tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sup {minus}}{pi}{sup +}{pi}{sup {minus}} events, we examine the resonance structure of the K{sup {minus}}{pi}{sup +}{pi}{sup {minus}} system and obtain the first measurements of branching fractions for {tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sub 1}{sup {minus}}(1270) and {tau}{sup {minus}} {yields} {nu}{sub {tau}}K{sub 1}{sup {minus}}(1400). We also describe a complete set of branching fraction measurements in which all the decays of the {tau}{sup {minus}} lepton are separated into classes defined by the identities of the charged particles and an estimate of the number of neutrals. This is the first such global measurement with decay classes defined by the four possible charged particle species, e, {mu}, {pi}, and K.

  2. Search for neutral Higgs bosons decaying to tau pairs in association with b-quarks at the D0 Detector

    SciTech Connect

    Herner, Kenneth

    2009-06-01

    We report results from a search for neutral Higgs bosons decaying to tau pairs produced in association with a b-quark in 1.2 fb{sup -1} of data taken from June 2006 to August 2007 with the D0 detector at Fermi National Accelerator Laboratory. The final state includes a muon, hadronically decaying tau and jet identified as coming from a b-quark. We set cross section times branching ratio limits on production of such neutral Higgs bosons {phi} in the mass range from 90 GeV/c{sup 2} to 160 GeV/c{sup 2}. Exclusion limits are set at the 95% Confidence Level for several supersymmetric scenarios.

  3. Search for MSSM Higgs decaying to tau pairs in ppbar collision at s**(1/2) = 1.96 TeV at CDF

    SciTech Connect

    Jang, Dongwook

    2006-05-01

    This thesis presents the search for neutral Minimal Supersymmetric extension of Standard Model (MSSM) Higgs bosons decaying to tau pairs where one of the taus decays leptonically, and the other one hadronically. CDF Run II data with L{sub int} = 310 pb{sup -1} are used. There is no evidence of MSSM Higgs existence, which results in the upper limits on {sigma}(p{bar p} {yields} {phi}) x BR({phi} {yields} {tau}{tau}) in m{sub A} range between 115 and 250 GeV. These limits exclude some area in tan {beta} vs m{sub A} parameter space.

  4. Bilocal expansion of the Borel amplitude and the hadronic tau decay width

    SciTech Connect

    Cvetic, Gorazd; Lee, Taekoon

    2001-07-01

    The singular part of the Borel transform of a QCD amplitude near the infrared renormalon can be expanded in terms of higher order Wilson coefficients of the operators associated with the renormalon. In this paper we observe that this expansion gives nontrivial constraints on the Borel amplitude that can be used to improve the accuracy of the ordinary perturbative expansion of the Borel amplitude. In particular, we consider the Borel transform of the Adler function and its expansion around the first infrared renormalon due to the gluon condensate. Using the next-to-leading order (NLO) Wilson coefficient of the gluon condensate operator, we obtain an exact constraint on the Borel amplitude at the first IR renormalon. We then extrapolate, using judiciously chosen conformal transformations and Pade{prime} approximants, the ordinary perturbative expansion of the Borel amplitude in such a way that this constraint is satisfied. This procedure allows us to predict the O({alpha}{sub s}{sup 4}) coefficient of the Adler function, which gives a result consistent with the estimate by Kataev and Starshenko using a completely different method. We then apply this improved Borel amplitude to the tau decay width and obtain the strong coupling constant {alpha}{sub s}(M{sub z}{sup 2})=0.1193{+-}0.0007{sub exp.}{+-}0.0010{sub EW+CKM}{+-}0.0009{sub meth.}{+-}0.0003{sub evol.}. We then compare this result with those of other resummation methods.

  5. Search for lepton flavor violating decay $\\tau^- \\to \\ell^- \\ell^ \\ell^-$ at BaBar

    SciTech Connect

    Cervelli, Alberto

    2010-05-26

    The Standard Model (SM) is one of the most tested and verified physical theories of all time, present experimental observations are consistent with SM expectations. On the other hand SM can not explain many physical observations: the cosmological observations possibly infer the presence of dark matter which is clearly beyond the SM expectations; the SM Higgs model, while explaining the generation of fermion masses, can not explain the hierarchy problem and a non natural fine tuning of SM is needed to cancel out quadratic divergences in the Higgs boson mass. New physics (NP) beyond SM should hence be investigated: rising the energy above NP processes thresholds, and detecting new particles or new effects not predicted by the standard model directly, is one of the possible approaches; another approach is to make precision measurements of well known processes or looking for rare processes which involve higher order contribution from NP processes, this approach need higher luminosities with respect to the previous approach but lower beam energies. Search for Lepton Flavor Violation (LFV) in charged lepton decays is promising: neutrino physics provides indeed a clear and unambiguous evidence of LFV in the neutral lepton sector via mixing processes, which have been observed for the first time by the Homestake collaboration. We expect LFV in the charged sector as well, both in {mu} and {tau} sector, but current experimental searches for LFV processes did not find any evidence for those processes, and more results are expected to come from new experiments in the coming years.

  6. A Search for Supersymmetric Higgs Bosons in the Di-tau Decay Mode in Proton - Anti-proton Collisions at 1.8 TeV

    SciTech Connect

    Connolly, Amy Lynn

    2003-09-01

    A search for directly produced Supersymmetric Higgs Bosons has been performed in the di-tau decay channel in 86.3 {+-} 3.5 pb{sup -1} of data collected by CDF during Run1b at the Tevatron. They search for events where one tau decays to an electron and the other tau decays hadronically. They perform a counting experiment and set limits on the cross section for Higgs production in the high tan {beta} region of the m{sub A}-tan {beta} plane. For a benchmark parameter space point where m{sub A} = 100 and tan {beta} = 50, they set a 95% confidence level upper limit at 891 pb compared to the theoretically predicted cross section of 122 pb. For events where the tau candidates are not back-to-back, they utilize a di-tau mass reconstruction technique for the first time on hadron collider data. Limits based on a likelihood binned in di-tau mass from non-back-to-back events alone are weaker than the limits obtained from the counting experiment using the full di-tau sample.

  7. Tau Biology and Tau-Directed Therapies for Alzheimer's Disease.

    PubMed

    Bakota, Lidia; Brandt, Roland

    2016-03-01

    Alzheimer's disease (AD) is characterised by a progressive loss of cognitive functions. Histopathologically, AD is defined by the presence of extracellular amyloid plaques containing A? and intracellular neurofibrillary tangles composed of hyperphosphorylated tau proteins. According to the now well-accepted amyloid cascade hypothesis is the A? pathology the primary driving force of AD pathogenesis, which then induces changes in tau protein leading to a neurodegenerative cascade during the progression of disease. Since many earlier drug trials aiming at preventing A? pathology failed to demonstrate efficacy, tau and microtubules have come into focus as prominent downstream targets. The article aims to develop the current concept of the involvement of tau in the neurodegenerative triad of synaptic loss, cell death and dendritic simplification. The function of tau as a microtubule-associated protein and versatile interaction partner will then be introduced and the rationale and progress of current tau-directed therapy will be discussed in the biological context. PMID:26729186

  8. Anesthesia and Tau Pathology

    PubMed Central

    Whittington, Robert A.; Bretteville, Alexis; Dickler, Maya F.; Planel, Emmanuel

    2013-01-01

    Alzheimer’s disease (AD) is the most common form of dementia and remains a growing worldwide health problem. As life expectancy continues to increase, the number of AD patients presenting for surgery and anesthesia will steadily rise. The etiology of sporadic AD is thought to be multifactorial, with environmental, biological and genetic factors interacting together to influence AD pathogenesis. Recent reports suggest that general anesthetics may be such a factor and may contribute to the development and exacerbation of this neurodegenerative disorder. Intra-neuronal neurofibrillary tangles (NFT), composed of hyperphosphorylated and aggregated tau protein are one of the main neuropathological hallmarks of AD. Tau pathology is important in AD as it correlates very well with cognitive dysfunction. Lately, several studies have begun to elucidate the mechanisms by which anesthetic exposure might affect the phosphorylation, aggregation and function of this microtubule-associated protein. Here, we specifically review the literature detailing the impact of anesthetic administration on aberrant tau hyperphosphorylation as well as the subsequent development of neurofibrillary pathology and degeneration. PMID:23535147

  9. A Search for B+ to tau+ nu

    SciTech Connect

    Aubert, B.

    2007-06-26

    The authors present a search for the decay B{sup +} {yields} {tau}{sup +}{nu} using 383 x 10{sup 6} B{bar B} pairs collected at the {Upsilon}(4S) resonance with the BABAR detector at the SLAC PEP-II B-Factory. A sample of events with one reconstructed semileptonic B decay (B{sup -} {yields} D{sup 0}{ell}{sup -}{bar {nu}}{sub {ell}}X) is selected, and in the recoil a search for B{sup +} {yields} {tau}{sup +}{nu} is performed. The {tau} is identified in the following channels: {tau}{sup +} {yields} e{sup +}{nu}{bar {nu}}, {tau}{sup +} {yields} {mu}{sup +}{nu}{bar {nu}}, {tau}{sup +} {yields} {pi}{sup +} {bar {nu}} and {tau}{sup +} {yields} {pi}{sup +}{pi}{sup 0}{bar {nu}}. They measure a branching fraction of {Beta}(B{sup +} {yields} {tau}{sup +}{nu}) = (0.9 {+-} 0.6(stat.) {+-} 0.1(syst.)) x 10{sup -4}. In the absence of a significant signal, we calculate an upper limit at the 90% confidence level of {Beta}(B{sup +} {yields} {tau}{sup +}{nu}) < 1.7 x 10{sup -4}. They calculate the product of the B meson decay constant f{sub B} and |V{sub ub}| to be f{sub B} {center_dot} |V{sub ub}| = (7.2{sub -2.8}{sup +2.0}(stat.) {+-} 0.2(syst.)) x 10{sup -4} GeV.

  10. Search for the charged Higgs boson in the decays of top quark pairs in the e{tau} and {mu}{tau} channels at {radical}( s )=1.8 TeV

    SciTech Connect

    Affolder, T.; Akimoto, H.; Akopian, A.; Albrow, M. G.; Amaral, P.; Amendolia, S. R.; Amidei, D.; Anikeev, K.; Antos, J.; Apollinari, G.

    2000-07-01

    Top quark production offers the unique opportunity to search for a charged Higgs boson (H{sup {+-}}), as the contribution from t{yields}H{sup +}b{yields}{tau}{sup +}{nu}b can be large in extensions of the standard model. We use results from a search for top quark pair production by the Collider Detector at Fermilab (CDF) in the e{tau}+Ee{sub T}+jets and {mu}{tau}+Ee{sub T}+jets signatures to set an upper limit on the branching ratio of B(t{yields}H{sup +}b) in 106 pb{sup -1} of data. The upper limit is in the range 0.5 to 0.6 at 95% C.L. for H{sup +} masses in the range 60 to 160 GeV, assuming the branching ratio for H{sup +}{yields}{tau}{nu} is 100%. The {tau} lepton is detected through its 1-prong and 3-prong hadronic decays. (c) 2000 The American Physical Society.

  11. Measurement of the Tau Lepton Lifetime with BaBar

    SciTech Connect

    Lusiani, A.; /Pisa, Scuola Normale Superiore /INFN, Pisa

    2005-06-27

    The mean lifetime of the tau lepton is measured from the decay length distribution of 3-prong tau decays from e{sup +}e{sup -} collisions at the {Upsilon}(4S) resonance. A data sample of 80.0 fb{sup -1} collected with the BABAR detector at the PEP-II B Factory is used for this measurement. The measured tau lifetime is: {tau}{sub {tau}} = 289.40 {+-} 0.91 (stat.) {+-} 0.90 (syst.) fs. All the results are preliminary.

  12. A study of w boson decay charge asymmetry using hadronic tau decays in proton - anti-proton collisions at {radical}s = 1.8 TeV

    SciTech Connect

    E.W Kuns

    2002-10-18

    This dissertation presents a measurement of the tau charge asymmetry in events where the taus are produced by W decays. This charge asymmetry appears as different rapidity distributions for positive and negative taus. Two competing effects generate tau charge asymmetry. The production mechanism for the W gauge boson generates a charge asymmetry which is a function of the ratio of parton distribution functions, d(x)=u(x), measured at x {approx} M{sub W}/{radical}s. This is the dominant effect for tau charge asymmetry at small rapidity. At higher rapidity, however, the competing charge asymmetry from parity violation in W decay to taus becomes dominant. This tau asymmetry measurement is consistent with the Standard Model with a x{sup 2} per degree of freedom equal to 2.5 for 4 degrees of freedom when the asymmetry measurement is folded about y = 0, taking advantage of the CP symmetry of the underlying physics, and 8.9 for 8 degrees of freedom when it is not. This measurement introduces some methods and variables of interest to future analyses using hadronic decay modes of taus. This work was done using the CDF detector in {bar p}p collisions at {radical} = 1.8 TeV at Fermilab's Tevatron accelerator.

  13. Tau immunization: a cautionary tale?

    PubMed

    Mably, Alexandra J; Kanmert, Daniel; Mc Donald, Jessica M; Liu, Wen; Caldarone, Barbara J; Lemere, Cynthia A; O'Nuallain, Brian; Kosik, Kenneth S; Walsh, Dominic M

    2015-03-01

    The amyloid ? (A?)-protein and microtubule-associated protein, tau, are the major components of the amyloid plaques and neurofibrillary tangles that typify Alzheimer's disease (AD) pathology. As such both A? and tau have long been proposed as therapeutic targets. Immunotherapy, particularly targeting A?, is currently the most advanced clinical strategy for treating AD. However, several A?-directed clinical trials have failed, and there is concern that targeting this protein may not be useful. In contrast, there is a growing optimism that tau immunotherapy may prove more efficacious. Here, for the first time, we studied the effects of chronic administration of an anti-tau monoclonal antibody (5E2) in amyloid precursor protein transgenic mice. For our animal model, we chose the J20 mouse line because prior studies had shown that the cognitive deficits in these mice require expression of tau. Despite the fact that 5E2 was present and active in the brains of immunized mice and that this antibody appeared to engage with extracellular tau, 5E2-treatment did not recover age-dependent spatial reference memory deficits. These results indicate that the memory impairment evident in J20 mice is unlikely to be mediated by a form of extracellular tau recognized by 5E2. In addition to the lack of positive effect of anti-tau immunotherapy, we also documented a significant increase in mortality among J20 mice that received 5E2. Because both the J20 mice used here and tau transgenic mice used in prior tau immunotherapy trials are imperfect models of AD our results recommend extensive preclinical testing of anti-tau antibody-based therapies using multiple mouse models and a variety of different anti-tau antibodies. PMID:25619661

  14. Developments in Tau PET Imaging.

    PubMed

    Zimmer, Eduardo Rigon; Leuzy, Antoine; Gauthier, Serge; Rosa-Neto, Pedro

    2014-09-01

    ABSTRACT The presence of neurofibrillary tangles in the brain is a hallmark feature of several neurodegenerative diseases termed "tauopathies," including Alzheimer's disease (AD) and the tau molecular subgroup of frontotemporal lobar degeneration (FTLD-tau). Recently, several positron emission tomography (PET) radiopharmaceuticals targeting abnormal conformations of the tau protein have been developed. To date, six novel tau imaging agents-[18F]THK523, [18F]THK5105, [18F]THK5117, [18F]T807, [18F]T808, and [11C]PBB3-have been described and are considered promising as potential tau radioligands. Tau imaging agents offer the opportunity of in vivo topographical mapping and quantification of tau aggregates in parallel with clinical and cognitive assessments. As such, tau imaging is considered of key importance for progress toward earlier and more accurate diagnosis of tauopathies as well as for the monitoring of therapeutic interventions and drug development. Here, we shed light on the most important developments in tau radiopharmaceuticals, highlighting challenges, possibilities and future directions. PMID:25424608

  15. Search for Neutral Minimal Supersymmetric Standard Model Higgs Bosons Decaying to Tau Pairs in pp Collisions at sqrt[s]=7 TeV

    SciTech Connect

    Chatrchyan, Serguei; et al.

    2011-06-01

    A search for neutral MSSM Higgs bosons in pp collisions at the LHC at a center-of-mass energy of 7 TeV is presented. The results are based on a data sample corresponding to an integrated luminosity of 36 inverse picobarns recorded by the CMS experiment. The search uses decays of the Higgs bosons to tau pairs. No excess is observed in the tau-pair invariant-mass spectrum. The resulting upper limits on the Higgs boson production cross section times branching fraction to tau pairs, as a function of the pseudoscalar Higgs boson mass, yield stringent new bounds in the MSSM parameter space.

  16. Study of top quark production and decays involving a tau lepton at CDF and limits on a charged Higgs boson contribution

    NASA Astrophysics Data System (ADS)

    Aaltonen, T.; Amerio, S.; Amidei, D.; Anastassov, A.; Annovi, A.; Antos, J.; Apollinari, G.; Appel, J. A.; Arisawa, T.; Artikov, A.; Asaadi, J.; Ashmanskas, W.; Auerbach, B.; Aurisano, A.; Azfar, F.; Badgett, W.; Bae, T.; Barbaro-Galtieri, A.; Barnes, V. E.; Barnett, B. A.; Barria, P.; Bartos, P.; Bauce, M.; Bedeschi, F.; Behari, S.; Bellettini, G.; Bellinger, J.; Benjamin, D.; Beretvas, A.; Bhatti, A.; Bland, K. R.; Blumenfeld, B.; Bocci, A.; Bodek, A.; Bortoletto, D.; Boudreau, J.; Boveia, A.; Brigliadori, L.; Bromberg, C.; Brucken, E.; Budagov, J.; Budd, H. S.; Burkett, K.; Busetto, G.; Bussey, P.; Butti, P.; Buzatu, A.; Calamba, A.; Camarda, S.; Campanelli, M.; Canelli, F.; Carls, B.; Carlsmith, D.; Carosi, R.; Carrillo, S.; Casal, B.; Casarsa, M.; Castro, A.; Catastini, P.; Cauz, D.; Cavaliere, V.; Cavalli-Sforza, M.; Cerri, A.; Cerrito, L.; Chen, Y. C.; Chertok, M.; Chiarelli, G.; Chlachidze, G.; Cho, K.; Chokheli, D.; Clark, A.; Clarke, C.; Convery, M. E.; Conway, J.; Corbo, M.; Cordelli, M.; Cox, C. A.; Cox, D. J.; Cremonesi, M.; Cruz, D.; Cuevas, J.; Culbertson, R.; d'Ascenzo, N.; Datta, M.; de Barbaro, P.; Demortier, L.; Deninno, M.; D'Errico, M.; Devoto, F.; Di Canto, A.; Di Ruzza, B.; Dittmann, J. R.; Donati, S.; D'Onofrio, M.; Dorigo, M.; Driutti, A.; Ebina, K.; Edgar, R.; Elagin, A.; Erbacher, R.; Errede, S.; Esham, B.; Farrington, S.; Fernndez Ramos, J. P.; Field, R.; Flanagan, G.; Forrest, R.; Franklin, M.; Freeman, J. C.; Frisch, H.; Funakoshi, Y.; Galloni, C.; Garfinkel, A. F.; Garosi, P.; Gerberich, H.; Gerchtein, E.; Giagu, S.; Giakoumopoulou, V.; Gibson, K.; Ginsburg, C. M.; Giokaris, N.; Giromini, P.; Giurgiu, G.; Glagolev, V.; Glenzinski, D.; Gold, M.; Goldin, D.; Golossanov, A.; Gomez, G.; Gomez-Ceballos, G.; Goncharov, M.; Gonzlez Lpez, O.; Gorelov, I.; Goshaw, A. T.; Goulianos, K.; Gramellini, E.; Grinstein, S.; Grosso-Pilcher, C.; Group, R. C.; Guimaraes da Costa, J.; Hahn, S. R.; Han, J. Y.; Happacher, F.; Hara, K.; Hare, M.; Harr, R. F.; Harrington-Taber, T.; Hatakeyama, K.; Hays, C.; Heinrich, J.; Herndon, M.; Hocker, A.; Hong, Z.; Hopkins, W.; Hou, S.; Hughes, R. E.; Husemann, U.; Hussein, M.; Huston, J.; Introzzi, G.; Iori, M.; Ivanov, A.; James, E.; Jang, D.; Jayatilaka, B.; Jeon, E. J.; Jindariani, S.; Jones, M.; Joo, K. K.; Jun, S. Y.; Junk, T. R.; Kambeitz, M.; Kamon, T.; Karchin, P. E.; Kasmi, A.; Kato, Y.; Ketchum, W.; Keung, J.; Kilminster, B.; Kim, D. H.; Kim, H. S.; Kim, J. E.; Kim, M. J.; Kim, S. H.; Kim, S. B.; Kim, Y. J.; Kim, Y. K.; Kimura, N.; Kirby, M.; Knoepfel, K.; Kondo, K.; Kong, D. J.; Konigsberg, J.; Kotwal, A. V.; Kreps, M.; Kroll, J.; Kruse, M.; Kuhr, T.; Kurata, M.; Laasanen, A. T.; Lammel, S.; Lancaster, M.; Lannon, K.; Latino, G.; Lee, H. S.; Lee, J. S.; Leo, S.; Leone, S.; Lewis, J. D.; Limosani, A.; Lipeles, E.; Lister, A.; Liu, H.; Liu, Q.; Liu, T.; Lockwitz, S.; Loginov, A.; Lucchesi, D.; Luc, A.; Lueck, J.; Lujan, P.; Lukens, P.; Lungu, G.; Lys, J.; Lysak, R.; Madrak, R.; Maestro, P.; Malik, S.; Manca, G.; Manousakis-Katsikakis, A.; Marchese, L.; Margaroli, F.; Marino, P.; Martnez, M.; Matera, K.; Mattson, M. E.; Mazzacane, A.; Mazzanti, P.; McNulty, R.; Mehta, A.; Mehtala, P.; Mesropian, C.; Miao, T.; Mietlicki, D.; Mitra, A.; Miyake, H.; Moed, S.; Moggi, N.; Moon, C. S.; Moore, R.; Morello, M. J.; Mukherjee, A.; Muller, Th.; Murat, P.; Mussini, M.; Nachtman, J.; Nagai, Y.; Naganoma, J.; Nakano, I.; Napier, A.; Nett, J.; Neu, C.; Nigmanov, T.; Nodulman, L.; Noh, S. Y.; Norniella, O.; Oakes, L.; Oh, S. H.; Oh, Y. D.; Oksuzian, I.; Okusawa, T.; Orava, R.; Ortolan, L.; Pagliarone, C.; Palencia, E.; Palni, P.; Papadimitriou, V.; Parker, W.; Pauletta, G.; Paulini, M.; Paus, C.; Phillips, T. J.; Piacentino, G.; Pianori, E.; Pilot, J.; Pitts, K.; Plager, C.; Pondrom, L.; Poprocki, S.; Potamianos, K.; Pranko, A.; Prokoshin, F.; Ptohos, F.; Punzi, G.; Ranjan, N.; Redondo Fernndez, I.; Renton, P.; Rescigno, M.; Rimondi, F.; Ristori, L.; Rizzi, C.; Robson, A.; Rodriguez, T.; Rolli, S.; Ronzani, M.; Roser, R.; Rosner, J. L.; Ruffini, F.; Ruiz, A.; Russ, J.; Rusu, V.; Sakumoto, W. K.; Sakurai, Y.; Santi, L.; Sato, K.; Saveliev, V.; Savoy-Navarro, A.; Schlabach, P.; Schmidt, E. E.; Schwarz, T.; Scodellaro, L.; Scuri, F.; Seidel, S.; Seiya, Y.; Semenov, A.; Sforza, F.; Shalhout, S. Z.; Shears, T.; Shepard, P. F.; Shimojima, M.; Shochet, M.; Shreyber-Tecker, I.; Simonenko, A.; Sliwa, K.; Smith, J. R.; Snider, F. D.; Song, H.; Sorin, V.; St. Denis, R.; Stancari, M.; Stentz, D.; Strologas, J.; Sudo, Y.; Sukhanov, A.; Suslov, I.; Takemasa, K.; Takeuchi, Y.; Tang, J.; Tecchio, M.; Teng, P. K.; Thom, J.; Thomson, E.; Thukral, V.; Toback, D.; Tokar, S.; Tollefson, K.; Tomura, T.; Tonelli, D.; Torre, S.; Torretta, D.; Totaro, P.; Trovato, M.; Ukegawa, F.; Uozumi, S.; Velev, G.

    2014-05-01

    We present an analysis of top-antitop quark production and decay into a tau lepton, tau neutrino, and bottom quark using data from 9 fb-1 of integrated luminosity at the Collider Detector at Fermilab. Dilepton events, where one lepton is an energetic electron or muon and the other a hadronically decaying tau lepton, originating from proton-antiproton collisions at ?s =1.96 TeV, are used. A top-antitop quark production cross section of 8.12.1 pb is measured, assuming standard-model top quark decays. By separately identifying for the first time the single-tau and the ditau components, we measure the branching fraction of the top quark into the tau lepton, tau neutrino, and bottom quark to be (9.62.8)%. The branching fraction of top quark decays into a charged Higgs boson and a bottom quark, which would imply violation of lepton universality, is limited to be less than 5.9% at a 95% confidence level [for B(H-???)=1].

  17. Modulation of tau pathology in tau transgenic models.

    PubMed

    Brion, Jean-Pierre; Ando, Kunie; Heraud, Cline; Leroy, Karelle

    2010-08-01

    NFTs (neurofibrillary tangles) in Alzheimer's disease and in tauopathies are hallmark neuropathological lesions whose relationship with neuronal dysfunction, neuronal death and with other lesions [such as Abeta (amyloid beta-peptide) pathology] are still imperfectly understood. Many transgenic mice overexpressing wild-type or mutant tau proteins have been generated to investigate the physiopathology of tauopathies. Most of the mice overexpressing wild-type tau do not develop NFTs, but can develop a severe axonopathy, whereas overexpression of mutant tau leads to NFT formation, synaptic loss and neuronal death in several models. The association between neuronal death and NFTs has, however, been challenged in some models showing a dissociation between tau aggregation and tau toxicity. Cross-breeding of mice developing NFTs with mice developing Abeta deposits increases NFT pathology, highlighting the relationship between tau and amyloid pathology. On the other hand, tau expression seems to be necessary for expression of a pathological phenotype associated with amyloid pathology. These findings suggest that there is a bilateral cross-talk between Abeta and tau pathology. These observations are discussed by the presentation of some relevant models developed recently. PMID:20658992

  18. UX Tau A

    NASA Technical Reports Server (NTRS)

    2007-01-01

    This is an artist's rendition of the one-million-year-old star system called UX Tau A, located approximately 450 light-years away. Observations from NASA's Spitzer Space Telescope showed a gap in the dusty planet-forming disk swirling around the system's central sun-like star.

    Spitzer saw a gap in UX Tau A's disk that extends from 0.2 to 56 astronomical units (an astronomical unit is the distance between the sun and Earth). The gap extends from the equivalent of Mercury to Pluto in our solar system, and is sandwiched between thick inner and outer disks on either side. Astronomers suspect that the gap was carved out by one or more forming planets.

    Such dusty disks are where planets are thought to be born. Dust grains clump together like snowballs to form larger rocks, and then the bigger rocks collide to form the cores of planets. When rocks revolve around their central star, they act like cosmic vacuum cleaners, picking up all the gas and dust in their path and creating gaps.

    Although gaps have been detected in disks swirling around young stars before, UX Tau A is special because the gap is sandwiched between two thick disks of dust. An inner thick dusty disk hugs the central star, then, moving outward, there is a gap, followed by another thick doughnut-shaped disk. Other systems with gaps contain very little to no dust near the central star. In other words, those gaps are more like big holes in the centers of disks.

    Some scientists suspect that these holes could have been carved out by a process called photoevaporation. Photoevaporation occurs when radiation from the central star heats up the gas and dust around it to the point where it evaporates away. The fact that there is thick disk swirling extremely close to UX Tau A's central star rules out the photoevaporation scenario. If photoevaporation from the star played a role, then large amounts of dust would not be floating so close to the star.

  19. Search for Neutral MSSM Higgs Bosons Decaying to Pairs of Tau Leptons at Center of Mass Energy = 7 TeV

    NASA Astrophysics Data System (ADS)

    Friis, Evan Klose

    2011-12-01

    This thesis describes a search for the Higgs boson, a new particle predicted by a theory called the minimal supersymmetric extension to the standard model (MSSM). The standard model of particle physics, the MSSM, and Higgs boson phenomenology are introduced briefly. The search presented in this thesis uses a single final state configuration, in which the Higgs boson decays to two tau leptons, with one tau decaying to a muon and neutrinos, and the other decaying to pions and a single neutrino. Two new methods are introduced in this analysis, the Tau Neural Classifier tau identification algorithm, and the Secondary Vertex fit tau pair mass reconstruction method. Both methods are discussed in detail. The analysis uses the 2010 dataset from the Compact Muon Solenoid (CMS) experiment, which contains 36 pb-1 of integrated luminosity at a center of mass energy of 7 TeV. In total, 573 events are selected in the analysis. We fit the observed tau pair mass spectrum and measure the composition of the events. The result is compatible with the standard model expectation. No excess of signal events is observed, and we set an upper limit on the cross section times branching ratio of a Higgs boson. This limit is interpreted in the parameter space of the MSSM.

  20. Horizontal Tau air showers from mountains in deep vally :Traces of Ultrahigh neutrino tau

    NASA Astrophysics Data System (ADS)

    Fargion, Daniele

    1999-08-01

    Ultra High Energy (UHE) Tau neutrino may lead to a very peculiar imprint in future underground K m3 detectors in water and ice as well as in air: rarest secondary tau tracks and decay which may exceed the muon ones. Indeed Bremsstrahlung at high energy lead to longer tracks for heavier leptons. Radiation lenght grows nearly with the square of the lepton mass. Indeed electrons are too light and their trace in matter is negligible (decimeters) muon are much better observed, while tau are too short life time and short range to be found. However, because relativistic time expansion, UHE tau traces in matter, above 1017 eV , are relativistically boosted overcoming the corresponding muon tracks, already bounded by bremsstrahlung logaritmic regime. The tau crossing for Kms in water or ice may be confused with common muon tracks; their tau decay may be missunderstood as muonic catastrophic brehmstrallung interactions. To economize UHE tau dicovery, we suggest to look the tau decay in air into the deep valleys montains, like Canyons or deep in escavation mines where horizontal air showers induce fluoresce or Cerenkov lights. The mountain valley width screens from horizontal secondary muons. The valley height increases the solid angle view. The horizontal air Kms-size gap offer a strong discriminator to filter UHE muons against tau. Tens event a year at PeV ( W resonance peak) energies in K m3 excavation gap should be observable . Hunting air shower in the night toward high mountains in Canyons or in a deep excavation may be the best and cheapest way to discover UHE neutrinos , either born by electron antineutrino scattering on electrons at PeV energies, or by direct tau neutrino possibly relic of muonic flavour oscillation even at EeV energies.

  1. Search for Second-Class Currents in tau- -> omega.pi-.nu_tau

    SciTech Connect

    Aubert, B.

    2009-04-22

    We report an analysis of {tau}{sup -} decaying into {omega}{pi}{sup -} {nu}{sub {tau}} with {omega} {yields} {pi}{sup +}{pi}{sup -}{pi}{sup 0} using a data sample containing nearly 320 million {tau} pairs collected with the BABAR detector at the PEP-II B-Factory. We find no evidence for second-class currents and we set an upper limit of 0.69% at 90% confidence level for the fraction of second-class currents in this decay mode.

  2. Test of the exponential decay law at short decay times using tau leptons

    NASA Astrophysics Data System (ADS)

    Alexander, G.; Allison, J.; Altekamp, N.; Ametewee, K.; Anderson, K. J.; Anderson, S.; Arcelli, S.; Asai, S.; Axen, D.; Azuelos, G.; Ball, A. H.; Barberio, E.; Barlow, R. J.; Bartoldus, R.; Batley, J. R.; Beaudoin, G.; Bechtluft, J.; Beck, G. A.; Beeston, C.; Behnke, T.; Bell, A. N.; Bell, K. W.; Bella, G.; Bentvelsen, S.; Berlich, P.; Bethke, S.; Biebel, O.; Bloodworth, I. J.; Bloomer, J. E.; Bock, P.; Bosch, H. M.; Boutemeur, M.; Bouwens, B. T.; Braibant, S.; Bright-Thomas, P.; Brown, R. M.; Burckhart, H. J.; Burgard, C.; Brgin, R.; Capiluppi, P.; Carnegie, R. K.; Carter, A. A.; Carter, J. R.; Chang, C. Y.; Charlesworth, C.; Charlton, D. G.; Chrisman, D.; Chu, S. L.; Clarke, P. E. L.; Clowes, S. G.; Cohen, I.; Conboy, J. E.; Cooke, O. C.; Cuffiani, M.; Dado, S.; Dallapiccola, C.; Dallavalle, G. M.; Darling, C.; De Jong, S.; del Pozo, L. A.; Dixit, M. S.; do Couto e Silva, E.; Duchovni, E.; Duckeck, G.; Duerdoth, I. P.; Dunwoody, U. C.; Edwards, J. E. G.; Estabrooks, P. G.; Evans, H. G.; Fabbri, F.; Fabbro, B.; Fath, P.; Fiedler, F.; Fierro, M.; Fincke-Keeler, M.; Fischer, H. M.; Folman, R.; Fong, D. G.; Foucher, M.; Fukui, H.; Frtjes, A.; Gagnon, P.; Gaidot, A.; Gary, J. W.; Gascon, J.; Gascon-Shotkin, S. M.; Geddes, N. I.; Geich-Gimbel, C.; Gensler, S. W.; Gentit, F. X.; Geralis, T.; Giacomelli, G.; Giacomelli, P.; Giacomelli, R.; Gibson, V.; Gibson, W. R.; Gingrich, D. M.; Goldberg, J.; Goodrick, M. J.; Gorn, W.; Grandi, C.; Gross, E.; Hajdu, C.; Hanson, G. G.; Hansroul, M.; Hapke, M.; Hargrove, C. K.; Hart, P. A.; Hartmann, C.; Hauschild, M.; Hawkes, C. M.; Hawkings, R.; Hemingway, R. J.; Herten, G.; Heuer, R. D.; Hildreth, M. D.; Hill, J. C.; Hillier, S. J.; Hilse, T.; Hobson, P. R.; Hochman, D.; Homer, R. J.; Honma, A. K.; Horvth, D.; Howard, R.; Hughes-Jones, R. E.; Hutchcroft, D. E.; Igo-Kemenes, P.; Imrie, D. C.; Jawahery, A.; Jeffreys, P. W.; Jeremie, H.; Jimack, M.; Joly, A.; Jones, M.; Jones, R. W. L.; Jost, U.; Jovanovic, P.; Karlen, D.; Kawamoto, T.; Keeler, R. K.; Kellogg, R. G.; Kennedy, B. W.; King, B. J.; King, J.; Kirk, J.; Kluth, S.; Kobayashi, T.; Kobel, M.; Koetke, D. S.; Kokott, T. P.; Komamiya, S.; Kowalewski, R.; Kress, T.; Krieger, P.; von Krogh, J.; Kyberd, P.; Lafferty, G. D.; Lafoux, H.; Lahmann, R.; Lai, W. P.; Lanske, D.; Lauber, J.; Layter, J. G.; Lee, A. M.; Lefebvre, E.; Lellouch, D.; Letts, J.; Levinson, L.; Lewis, C.; Lloyd, S. L.; Loebinger, F. K.; Long, G. D.; Lorazo, B.; Losty, M. J.; Ludwig, J.; Luig, A.; Malik, A.; Mannelli, M.; Marcellini, S.; Markus, C.; Martin, A. J.; Martin, J. P.; Martinez, G.; Mashimo, T.; Matthews, W.; Mttig, P.; McDonald, W. J.; McKenna, J.; Mckigney, E. A.; McMahon, T. J.; McNab, A. I.; Meijers, F.; Menke, S.; Merritt, F. S.; Mes, H.; Meyer, J.; Michelini, A.; Mikenberg, G.; Miller, D. J.; Mir, R.; Mohr, W.; Montanari, A.; Mori, T.; Morii, M.; Mller, U.; Nellen, B.; Nijjhar, B.; Nisius, R.; O'Neale, S. W.; Oakham, F. G.; Odorici, F.; Ogren, H. O.; Oldershaw, N. J.; Omori, T.; Oram, C. J.; Oreglia, M. J.; Orito, S.; Palazzo, M.; Plinks, J.; Palmonari, F. M.; Pansart, J. P.; Psztor, G.; Pater, J. R.; Patrick, G. N.; Pearce, M. J.; Phillips, P. D.; Pilcher, J. E.; Pinfold, J.; Plane, D. E.; Poffenberger, P.; Poli, B.; Posthaus, A.; Pritchard, T. W.; Przysiezniak, H.; Rees, D. L.; Rigby, D.; Rison, M. G.; Robins, S. A.; Rodning, N.; Roney, J. M.; Ros, E.; Rossi, A. M.; Rosvick, M.; Routenburg, P.; Rozen, Y.; Runge, K.; Runolfsson, O.; Rust, D. R.; Rylko, R.; Sarkisyan, E. K. G.; Sasaki, M.; Sbarra, C.; Schaile, A. D.; Schaile, O.; Scharf, F.; Scharff-Hansen, P.; Schenk, P.; Schmitt, B.; Schrder, M.; Schultz-Coulon, H. C.; Schulz, M.; Schtz, P.; Schwiening, J.; Scott, W. G.; Shears, T. G.; Shen, B. C.; Shepherd-Themistocleous, C. H.; Sherwood, P.; Siroli, G. P.; Sittler, A.; Skillman, A.; Skuja, A.; Smith, A. M.; Smith, T. J.; Snow, G. A.; Sobie, R.; Sldner-Rembold, S.; Springer, R. W.; Sproston, M.; Stahl, A.; Starks, M.; Stegmann, C.; Stephens, K.; Steuerer, J.; Stockhausen, B.; Strom, D.; Strumia, F.; Szymanski, P.; Tafirout, R.; Takeda, H.; Taras, P.; Tarem, S.; Tecchio, M.; Tesch, N.; Thomson, M. A.; von Trne, E.; Towers, S.; Tscheulin, M.; Tsukamoto, T.; Tsur, E.; Turcot, A. S.; Turner-Watson, M. F.; Utzat, P.; Van Kooten, R.; Vasseur, G.; Vikas, P.; Vincter, M.; Vokurka, E. H.; Wckerle, F.; Wagner, A.; Wagner, D. L.; Ward, C. P.; Ward, D. R.; Ward, J. J.; Watkins, P. M.; Watson, A. T.; Watson, N. K.; Weber, P.; Wells, P. S.; Wermes, N.; Wilkens, B.; Wilson, G. W.; Wilson, J. A.; Wlodek, T.; Wolf, G.; Wotton, S.; Wyatt, T. R.; Xella, S.; Yamashita, S.; Yekutieli, G.; Zacek, V.; OPAL Collaboration

    1996-02-01

    Quantum mechanics predicts an exponential distribution for the decay time of massive particles. However, deviations are expected for decay times shorter than about 10 -13 s in models conjecturing the existence of hidden variables. Following a recent proposal, the decay length distribution of 5843 ? leptons decaying into 3 charged particles was analyzed in search of such a deviation. The deviation from an exponential distribution with respect to the number of decays present within the exponential form, expressed as the relative weight of an excess at zero decay length, was measured to be 1.1%1.4%3.5%. This result is consistent with zero deviation and leads to an upper limit of 8.5% and a lower limit of -6.3% at the 95% confidence level.

  3. Results on Tau Physics from BABAR

    SciTech Connect

    Torrence, E.

    2004-10-29

    Recent results on tau physics from BABAR are reviewed. Limits on lepton-flavor violation in the tau decay process {tau}{sup -} {yields} {ell}{sup -}{ell}{sup +}{ell}{sup -} are presented based on 91.6 fb{sup -1} of data. In all six decay modes considered, the numbers of events found in data are compatible with the background expectations, and upper limits on the branching fractions are set in the range (1-3) x 10{sup -7} at 90% CL. A preliminary measurement of the .ve prong branching fraction based on 110.7 fb{sup -1} of data is presented with the result {Beta}({tau}{sup -} {yields} 3h{sup -}2h{sup +}{nu}{sub {tau}}) = (8.52 {+-} 0.09 {+-} 0.40) x 10{sup -4} . A preliminary measurement of the tau lifetime based on 30 fb{sup -1} of data is presented where a lifetime of 290.8 {+-} 1.5 {+-} 1.6 fs is measured.

  4. Search for lepton flavor violating decays tau(+/-) --> l(+/-)pi0, l(+/-)eta, l(+/-)eta'.

    PubMed

    Aubert, B; Bona, M; Boutigny, D; Couderc, F; Karyotakis, Y; Lees, J P; Poireau, V; Tisserand, V; Zghiche, A; Grauges, E; Palano, A; Chen, J C; Qi, N D; Rong, G; Wang, P; Zhu, Y S; Eigen, G; Ofte, I; Stugu, B; Abrams, G S; Battaglia, M; Brown, D N; Button-Shafer, J; Cahn, R N; Charles, E; Gill, M S; Groysman, Y; Jacobsen, R G; Kadyk, J A; Kerth, L T; Kolomensky, Yu G; Kukartsev, G; Lopes Pegna, D; Lynch, G; Mir, L M; Orimoto, T J; Pripstein, M; Roe, N A; Ronan, M T; Wenzel, W A; Del Amo Sanchez, P; Barrett, M; Ford, K E; Harrison, T J; Hart, A J; Hawkes, C M; Watson, A T; Held, T; Koch, H; Lewandowski, B; Pelizaeus, M; Peters, K; Schroeder, T; Steinke, M; Boyd, J T; Burke, J P; Cottingham, W N; Walker, D; Asgeirsson, D J; Cuhadar-Donszelmann, T; Fulsom, B G; Hearty, C; Knecht, N S; Mattison, T S; McKenna, J A; Khan, A; Kyberd, P; Saleem, M; Sherwood, D J; Teodorescu, L; Blinov, V E; Bukin, A D; Druzhinin, V P; Golubev, V B; Onuchin, A P; Serednyakov, S I; Skovpen, Yu I; Solodov, E P; Todyshev, K Yu; Best, D S; Bondioli, M; Bruinsma, M; Chao, M; Curry, S; Eschrich, I; Kirkby, D; Lankford, A J; Lund, P; Mandelkern, M; Roethel, W; Stoker, D P; Abachi, S; Buchanan, C; Foulkes, S D; Gary, J W; Long, O; Shen, B C; Wang, K; Zhang, L; Hadavand, H K; Hill, E J; Paar, H P; Rahatlou, S; Sharma, V; Berryhill, J W; Campagnari, C; Cunha, A; Dahmes, B; Hong, T M; Kovalskyi, D; Richman, J D; Beck, T W; Eisner, A M; Flacco, C J; Heusch, C A; Kroseberg, J; Lockman, W S; Nesom, G; Schalk, T; Schumm, B A; Seiden, A; Spradlin, P; Williams, D C; Wilson, M G; Albert, J; Chen, E; Cheng, C H; Dvoretskii, A; Fang, F; Hitlin, D G; Narsky, I; Piatenko, T; Porter, F C; Mancinelli, G; Meadows, B T; Mishra, K; Sokoloff, M D; Blanc, F; Bloom, P C; Chen, S; Ford, W T; Hirschauer, J F; Kreisel, A; Nagel, M; Nauenberg, U; Olivas, A; Ruddick, W O; Smith, J G; Ulmer, K A; Wagner, S R; Zhang, J; Chen, A; Eckhart, E A; Soffer, A; Toki, W H; Wilson, R J; Winklmeier, F; Zeng, Q; Altenburg, D D; Feltresi, E; Hauke, A; Jasper, H; Merkel, J; Petzold, A; Spaan, B; Brandt, T; Klose, V; Lacker, H M; Mader, W F; Nogowski, R; Schubert, J; Schubert, K R; Schwierz, R; Sundermann, J E; Volk, A; Bernard, D; Bonneaud, G R; Latour, E; Thiebaux, Ch; Verderi, M; Clark, P J; Gradl, W; Muheim, F; Playfer, S; Robertson, A I; Xie, Y; Andreotti, M; Bettoni, D; Bozzi, C; Calabrese, R; Cibinetto, G; Luppi, E; Negrini, M; Petrella, A; Piemontese, L; Prencipe, E; Anulli, F; Baldini-Ferroli, R; Calcaterra, A; de Sangro, R; Finocchiaro, G; Pacetti, S; Patteri, P; Peruzzi, I M; Piccolo, M; Rama, M; Zallo, A; Buzzo, A; Contri, R; Lo Vetere, M; Macri, M M; Monge, M R; Passaggio, S; Patrignani, C; Robutti, E; Santroni, A; Tosi, S; Brandenburg, G; Chaisanguanthum, K S; Lee, C L; Morii, M; Wu, J; Dubitzky, R S; Marks, J; Schenk, S; Uwer, U; Bard, D J; Bhimji, W; Bowerman, D A; Dauncey, P D; Egede, U; Flack, R L; Nash, J A; Nikolich, M B; Panduro Vazquez, W; Behera, P K; Chai, X; Charles, M J; Mallik, U; Meyer, N T; Ziegler, V; Cochran, J; Crawley, H B; Dong, L; Eyges, V; Meyer, W T; Prell, S; Rosenberg, E I; Rubin, A E; Gritsan, A V; Denig, A G; Fritsch, M; Schott, G; Arnaud, N; Davier, M; Grosdidier, G; Hcker, A; Lepeltier, V; Le Diberder, F; Lutz, A M; Oyanguren, A; Pruvot, S; Rodier, S; Roudeau, P; Schune, M H; Serrano, J; Stocchi, A; Wang, W F; Wormser, G; Lange, D J; Wright, D M; Chavez, C A; Forster, I J; Fry, J R; Gabathuler, E; Gamet, R; George, K A; Hutchcroft, D E; Payne, D J; Schofield, K C; Touramanis, C; Bevan, A J; Clarke, C K; Di Lodovico, F; Menges, W; Sacco, R; Cowan, G; Flaecher, H U; Hopkins, D A; Jackson, P S; McMahon, T R; Salvatore, F; Wren, A C; Brown, D N; Davis, C L; Allison, J; Barlow, N R; Barlow, R J; Chia, Y M; Edgar, C L; Lafferty, G D; Naisbit, M T; Williams, J C; Yi, J I; Chen, C; Hulsbergen, W D; Jawahery, A; Lae, C K; Roberts, D A; Simi, G; Blaylock, G; Dallapiccola, C; Hertzbach, S S; Li, X; Moore, T B; Saremi, S; Staengle, H; Cowan, R; Sciolla, G; Sekula, S J; Spitznagel, M; Taylor, F; Yamamoto, R K; Kim, H; McLachlin, S E; Patel, P M; Robertson, S H; Lazzaro, A; Lombardo, V; Palombo, F; Bauer, J M; Cremaldi, L; Eschenburg, V; Godang, R; Kroeger, R; Sanders, D A; Summers, D J; Zhao, H W; Brunet, S; Ct, D; Simard, M; Taras, P; Viaud, F B; Nicholson, H; Cavallo, N; De Nardo, G; Fabozzi, F; Gatto, C; Lista, L; Monorchio, D; Paolucci, P; Piccolo, D; Sciacca, C; Baak, M A; Raven, G; Snoek, H L; Jessop, C P; Losecco, J M; Benelli, G; Corwin, L A; Gan, K K; Honscheid, K; Hufnagel, D; Jackson, P D; Kagan, H; Kass, R; Rahimi, A M; Regensburger, J J; Ter-Antonyan, R; Wong, Q K; Blount, N L; Brau, J; Frey, R; Igonkina, O; Kolb, J A; Lu, M; Potter, C T; Rahmat, R; Sinev, N B; Strom, D; Strube, J; Torrence, E; Gaz, A; Margoni, M; Morandin, M; Pompili, A; Posocco, M; Rotondo, M; Simonetto, F; Stroili, R; Voci, C; Benayoun, M; Briand, H

    2007-02-01

    A search for lepton flavor violating decays of the tau lepton to a lighter mass lepton and a pseudoscalar meson has been performed using 339 fb;{-1} of e;{+}e;{-} annihilation data collected at a center-of-mass energy near 10.58 GeV by the BABAR detector at the SLAC PEP-II storage ring. No evidence of a signal has been found, and upper limits on the branching fractions are set at the 10;{-7} level. PMID:17358932

  5. Tau Lepton Mass Measurements

    SciTech Connect

    Lund, P.; /UC, Irvine

    2009-08-05

    The authors present the preliminary results from the precision measurement of the mass of the tau lepton using 423 fb{sup -1} of data collected at BABAR. Using a pseudomass endpoint method, they determine the mass to be 1776.68 {+-} 0.12(stat) {+-} 0.41(syst) MeV. They also measure the mass difference between the T{sup +} and T{sup -}, and obtain M{sub +}-M{sub -}/M{sub AVG} = (-3.5 {+-} 1.3) x 10{sup -4}. This results in a limit of -5.6 x 10{sup -4} < M{sub +}-M{sub -}/M{sub AVG} < -1.4 x 10{sup -4} at 90% CL.

  6. Sensitivity to the Higgs sector of supersymmetric-seesaw models in the lepton flavor violating {tau}{yields}{mu}f{sub 0}(980) decay

    SciTech Connect

    Herrero, M. J.; Rodriguez-Sanchez, A. M.

    2009-07-01

    In this work we study the lepton flavor violating (LFV) semileptonic {tau}{yields}{mu}f{sub 0}(980) decay within the context of SUSY-Seesaw Models, where the MSSM spectrum is extended by three right-handed neutrinos and their SUSY partners, and where the seesaw mechanism is used to generate the neutrino masses. We estimate its decay rate when it proceeds via the Higgs-mediated channel {tau}{yields}{mu}H{sup *}{yields}{mu}f{sub 0}(980), where H refers to the CP-even MSSM Higgs bosons h{sup 0} and H{sup 0}, and the lepton flavor violating {tau}{mu}H vertex is radiatively generated via SUSY loops. In order to describe the f{sub 0}(980) meson we follow the guidelines from chiral constraints. As an implication of our computation, we explore the sensitivity to the Higgs sector in this decay and compare it with other LFV tau decay channels. The confrontation of our predictions for BR({tau}{yields}{mu}f{sub 0}(980)) with its very competitive present experimental bound leads us to extract some interesting restrictions on the most relevant model parameters, particularly, tan{beta} and m{sub H{sup 0}}.

  7. Measurements of the {tau} mass and the mass difference of the {tau}{sup +} and {tau}{sup -} at BABAR

    SciTech Connect

    Aubert, B.; Karyotakis, Y.; Lees, J. P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D. N.; Kerth, L. T.; Kolomensky, Yu. G.; Lynch, G.

    2009-11-01

    We present the result from a precision measurement of the mass of the {tau} lepton, M{sub {tau}}, based on 423 fb{sup -1} of data recorded at the {upsilon}(4S) resonance with the BABAR detector. Using a pseudomass endpoint method, we determine the mass to be 1776.68{+-}0.12(stat){+-}0.41(syst) MeV. We also measure the mass difference between the {tau}{sup +} and {tau}{sup -}, and obtain (M{sub {tau}{sup +}}-M{sub {tau}{sup -}})/M{sub AVG}{sup {tau}}=(-3.4{+-}1.3(stat){+-}0.3(syst))x10{sup -4}, where M{sub AVG}{sup {tau}} is the average value of M{sub {tau}{sup +}} and M{sub {tau}{sup -}}.

  8. Time-weighted accumulations ap(. tau. ) and Kp(. tau. )

    SciTech Connect

    Wrenn, G.L. )

    1987-09-01

    The planetary geomagnetic indices Kp and ap are widely used in space geophysics. They provide an estimate of maximum magnetic perturbation within a 3-hour period. Many geophysical properties are clearly related to the indices, through energy transfer from a common disturbance source, but direct correlation is often lacking because of poor matching between the frequency of sampling and the physical response functions. The index ap({tau}) is a simple accumulation of the linear ap calculated with an attenuation factor {tau} included to take account of natural temporal relaxation. The case for ap({tau}) and the related Kp({tau}) is made using applications to the variability of the plasma environment in the ionosphere and inner magnetosphere. These examples of improved correlation suggest that time-weighted integration might profitably be applied to other indices.

  9. Photometric and spectroscopic monitoring of AA Tau, DN Tau, UX Tau A, T Tau, RY Tau, Lk Ca 4, and Lk Ca 7

    NASA Technical Reports Server (NTRS)

    Vrba, F. J.; Chugainov, P. F.; Weaver, W. B.; Stauffer, J. S.

    1993-01-01

    We report the results of a UBVRI photometric monitoring campaign for three classical T Tauri stars (AA Tau, DN Tau, and UX Tau A) and two weak emission line T Tauri stars (Lk Ca 4 and Lk Ca 7). Observations were obtained at three sites during a core observing period spanning UT 1985 October 14 through UT 1985 December 25, with additional observations continuing until UT 1986 April 6. Concurrent spectrophotometric observations were obtained for all main program stars except Lk Ca 7 and additionally for T Tau, RW Aur, and RY Tau. Periodic photometric variability, assumed to be the stars' rotation periods, were found for AA Tau, DN Tau, Lk Ca 4, and Lk Ca 7, respectively, as 8.2, 6.3, 3.4, and 5.7 days. Several U-filter flares were observed for Lk Ca 4 and Lk Ca 7, which are strongly concentrated toward phases of minimum light. Correlations are found between H-alpha line strengths and V magnitudes for AA Tau and RY Tau. An analysis of absolute color variations of classical T Tauri stars confirms that hot spots are the predominant cause of these stars' variability. Our overall results are consistent with earlier findings that long-lived cool spots are responsible for most of the variability found for weak-emission T Tauri stars, while temporal hot spots are primarily responsible for the observed variability found in classical T Tauri stars.

  10. Boronate-tau mediated uptake in neurons.

    PubMed

    Prez, Mar; Cuadros, Raquel; Pallas-Bazarra, Noemi; Garca, Carlos; Langa, Elena; Jurado-Arjona, Jernimo; Hernndez, Flix; Avila, Jess

    2014-01-01

    We modified tau protein with boronic acid to facilitate its delivery into non neural or neural cultured cells lacking tau protein. Our results indicate that the incorporated tau promotes the formation of cytoplasmic extensions in non-neuronal cells, as well as the appearance of neurites in cultured tau knockout hippocampal neurons. In addition, boronated tau is incorporated into hippocampal neurons of tau knockout mice after intracranial injection in vivo. These findings describe a novel method to deliver exogenous tau protein into cells. PMID:24366920

  11. Search for neutral Higgs bosons decaying to tau pairs produced in association with b-quarks at s**(1/2)=1.96 TeV

    SciTech Connect

    Herner, Kenneth Richard; /SUNY, Stony Brook

    2008-12-01

    We report results from a search for neutral Higgs bosons decaying to tau pairs produced in association with a b-quark in 1.6 fb{sup -1} of data taken from June 2006 to March 2008 with the D0 detector at Fermi National Accelerator Laboratory. The final state includes a muon, hadronically decaying tau, and jet identified as coming from a b-quark. We set cross section times branching ratio limits on production of such neutral Higgs bosons {phi} in the mass range from 90 GeV to 160 GeV. Exclusion limits are set at the 95% Confidence Level for several supersymmetric scenarios.

  12. Tau PET imaging in Alzheimer's disease.

    PubMed

    Okamura, Nobuyuki; Harada, Ryuichi; Furumoto, Shozo; Arai, Hiroyuki; Yanai, Kazuhiko; Kudo, Yukitsuka

    2014-11-01

    In several neurodegenerative diseases that are collectively called tauopathies, progressive accumulation of tau in the brain is closely associated with neurodegeneration and cognitive impairment. Noninvasive detection of tau protein deposits in the brain would be useful to diagnose tauopathies as well as to track and predict disease progression. Recently, several tau PET tracers including T807, THK-5117, and PBB3 have been developed and succeeded in imaging neurofibrillary pathology in vivo. For use of tau PET as a biomarker of tau pathology in Alzheimer's disease, PET tracers should have high affinity to PHF-tau and high selectivity for tau over amyloid-? and other protein deposits. PET tau imaging enables the longitudinal assessment of the spatial pattern of tau deposition and its relation to amyloid-? pathology and neurodegeneration. This technology could also be applied to the pharmacological assessment of anti-tau therapy, thereby allowing preventive interventions. PMID:25239654

  13. Therapeutic strategies for tau mediated neurodegeneration

    PubMed Central

    Yoshiyama, Yasumasa; Lee, Virginia M Y; Trojanowski, John Q

    2014-01-01

    Based on the amyloid hypothesis, controlling ?-amyloid protein (A?) accumulation is supposed to suppress downstream pathological events, tau accumulation, neurodegeneration and cognitive decline. However, in recent clinical trials, A? removal or reducing A? production has shown limited efficacy. Moreover, while active immunisation with A? resulted in the clearance of A?, it did not prevent tau pathology or neurodegeneration. This prompts the concern that it might be too late to employ A? targeting therapies once tau mediated neurodegeneration has occurred. Therefore, it is timely and very important to develop tau directed therapies. The pathomechanisms of tau mediated neurodegeneration are unclear but hyperphosphorylation, oligomerisation, fibrillisation and propagation of tau pathology have been proposed as the likely pathological processes that induce loss of function or gain of toxic function of tau, causing neurodegeneration. Here we review the strategies for tau directed treatments based on recent progress in research on tau and our understanding of the pathomechanisms of tau mediated neurodegeneration. PMID:23085937

  14. Closing the tau loop: the missing tau mutation.

    PubMed

    McCarthy, Allan; Lonergan, Roisin; Olszewska, Diana A; O'Dowd, Sean; Cummins, Gemma; Magennis, Brian; Fallon, Emer M; Pender, Niall; Huey, Edward D; Cosentino, Stephanie; O'Rourke, Killian; Kelly, Brendan D; O'Connell, Martin; Delon, Isabelle; Farrell, Michael; Spillantini, Maria Grazia; Rowland, Lewis P; Fahn, Stanley; Craig, Peter; Hutton, Michael; Lynch, Tim

    2015-10-01

    Frontotemporal lobar degeneration comprises a group of disorders characterized by behavioural, executive, language impairment and sometimes features of parkinsonism and motor neuron disease. In 1994 we described an Irish-American family with frontotemporal dementia linked to chromosome 17 associated with extensive tau pathology. We named this disinhibition-dementia-parkinsonism-amyotrophy complex. We subsequently identified mutations in the MAPT gene. Eleven MAPT gene splice site stem loop mutations were identified over time except for 5' splice site of exon 10. We recently identified another Irish family with autosomal dominant early amnesia and behavioural change or parkinsonism associated with the 'missing' +15 mutation at the intronic boundary of exon 10. We performed a clinical, neuropsychological and neuroimaging study on the proband and four siblings, including two affected siblings. We sequenced MAPT and performed segregation analysis. We looked for a biological effect of the tau variant by performing real-time polymerase chain reaction analysis of RNA extracted from human embryonic kidney cells transfected with exon trapping constructs. We found a c.915+15A>C exon 10/intron 10 stem loop mutation in all affected subjects but not in the unaffected. The c.915+15A>C variant caused a shift in tau splicing pattern to a predominantly exon 10+ pattern presumably resulting in predominant 4 repeat tau and little 3 repeat tau. This strongly suggests that the c.915+15A>C variant is a mutation and that it causes frontotemporal dementia linked to chromosome 17 in this pedigree by shifting tau transcription and translation to +4 repeat tau. Tau (MAPT) screening should be considered in families where amnesia or atypical parkinsonism coexists with behavioural disturbance early in the disease process. We describe the final missing stem loop tau mutation predicted 15 years ago. Mutations have now been identified at all predicted sites within the 'stem' when the stem-loop model was first proposed and no mutations have been found within the 'loop' region as expected. Therefore we 'close the tau loop' having 'opened the loop' 21 years ago. PMID:26297556

  15. Identification of disulfide cross-linked tau dimer responsible for tau propagation

    PubMed Central

    Kim, Dohee; Lim, Sungsu; Haque, Md. Mamunul; Ryoo, Nayeon; Hong, Hyun Seok; Rhim, Hyewhon; Lee, Dong-Eun; Chang, Young-Tae; Lee, Jun-Seok; Cheong, Eunji; Kim, Dong Jin; Kim, Yun Kyung

    2015-01-01

    Recent evidence suggests that tau aggregates are not only neurotoxic, but also propagate in neurons acting as a seed for native tau aggregation. Prion-like tau transmission is now considered as an important pathogenic mechanism driving the progression of tau pathology in the brain. However, prion-like tau species have not been clearly characterized. To identify infectious tau conformers, here we prepared diverse tau aggregates and evaluated the effect on inducing intracellular tau-aggregation. Among tested, tau dimer containing P301L-mutation is identified as the most infectious form to induce tau pathology. Biochemical analysis reveals that P301L-tau dimer is covalently cross-linked with a disulfide bond. The relatively small and covalently cross-linked tau dimer induced tau pathology efficiently in primary neurons and also in tau-transgenic mice. So far, the importance of tau disulfide cross-linking has been overlooked in the study of tau pathology. Here our results suggested that tau disulfide cross-linking might play critical role in tau propagation by producing structurally stable and small tau conformers. PMID:26470054

  16. Interaction of Tau with Fe65 links tau to APP.

    PubMed

    Barbato, Christian; Canu, Nadia; Zambrano, Nicola; Serafino, Annalucia; Minopoli, Giuseppina; Ciotti, Maria Teresa; Amadoro, Giuseppina; Russo, Tommaso; Calissano, Pietro

    2005-03-01

    The beta-amyloid precursor protein APP and the microtubule-associated protein Tau play a crucial role in the pathogenesis of Alzheimer's disease (AD). However, the possible molecular events linking these two proteins are still unknown. Here, we show that Fe65, one of the ligands of the APP cytodomain, is associated with Tau in vivo and in vitro, as demonstrated by co-immunoprecipitation, co-localization, and FRET experiments. Deletion studies indicated that the N-terminal domain of Tau and the PTB1 domain of Fe65 are required for this association. This interaction is regulated by the phosphorylation of Tau at selected sites, by glycogen synthase kinase-3beta (GSK3beta) and cyclin-dependent kinase 5 (Cdk5), and requires an intact microtubule network. Furthermore, laser scanner microscopy and co-immunoprecipitation experiments provide preliminary evidence of possible complex(es) involving Tau, Fe65, APP. These findings open new perspectives for the study of the possible crosstalk between these proteins in the pathogenesis of AD. PMID:15686969

  17. Accelerated Human Mutant Tau Aggregation by Knocking Out Murine Tau in a Transgenic Mouse Model

    PubMed Central

    Ando, Kunie; Leroy, Karelle; Hraud, Cline; Yilmaz, Zehra; Authelet, Michle; Suain, Valrie; De Decker, Robert; Brion, Jean-Pierre

    2011-01-01

    Many models of human tauopathies have been generated in mice by expression of a human mutant tau with maintained expression of mouse endogenous tau. Because murine tau might interfere with the toxic effects of human mutant tau, we generated a model in which a pathogenic human tau protein is expressed in the absence of wild-type tau protein, with the aim of facilitating the study of the pathogenic role of the mutant tau and to reproduce more faithfully a human tauopathy. The Tg30 line is a tau transgenic mouse model overexpressing human 1N4R double-mutant tau (P301S and G272V) that develops Alzheimer's disease-like neurofibrillary tangles in an age-dependent manner. By crossing Tg30 mice with mice invalidated for their endogenous tau gene, we obtained Tg30xtau?/? mice that express only exogenous human double-mutant 1N4R tau. Although Tg30xtau?/? mice express less tau protein compared with Tg30, they exhibit signs of decreased survival, increased proportion of sarkosyl-insoluble tau in the brain and in the spinal cord, increased number of Gallyas-positive neurofibrillary tangles in the hippocampus, increased number of inclusions in the spinal cord, and a more severe motor phenotype. Deletion of murine tau accelerated tau aggregation during aging of this mutant tau transgenic model, suggesting that murine tau could interfere with the development of tau pathology in transgenic models of human tauopathies. PMID:21281813

  18. Accelerated human mutant tau aggregation by knocking out murine tau in a transgenic mouse model.

    PubMed

    Ando, Kunie; Leroy, Karelle; Hraud, Cline; Yilmaz, Zehra; Authelet, Michle; Suain, Valrie; De Decker, Robert; Brion, Jean-Pierre

    2011-02-01

    Many models of human tauopathies have been generated in mice by expression of a human mutant tau with maintained expression of mouse endogenous tau. Because murine tau might interfere with the toxic effects of human mutant tau, we generated a model in which a pathogenic human tau protein is expressed in the absence of wild-type tau protein, with the aim of facilitating the study of the pathogenic role of the mutant tau and to reproduce more faithfully a human tauopathy. The Tg30 line is a tau transgenic mouse model overexpressing human 1N4R double-mutant tau (P301S and G272V) that develops Alzheimer's disease-like neurofibrillary tangles in an age-dependent manner. By crossing Tg30 mice with mice invalidated for their endogenous tau gene, we obtained Tg30xtau(-/-) mice that express only exogenous human double-mutant 1N4R tau. Although Tg30xtau(-/-) mice express less tau protein compared with Tg30, they exhibit signs of decreased survival, increased proportion of sarkosyl-insoluble tau in the brain and in the spinal cord, increased number of Gallyas-positive neurofibrillary tangles in the hippocampus, increased number of inclusions in the spinal cord, and a more severe motor phenotype. Deletion of murine tau accelerated tau aggregation during aging of this mutant tau transgenic model, suggesting that murine tau could interfere with the development of tau pathology in transgenic models of human tauopathies. PMID:21281813

  19. Tau Induces Cooperative Taxol Binding to Microtubules

    NASA Astrophysics Data System (ADS)

    Ross, Jennifer; Santangelo, Christian; Victoria, Makrides; Fygenson, Deborah

    2004-03-01

    Taxol and tau are two ligands which stabilize the microtubule (MT) lattice. Taxol is an anti-mitotic drug that binds ? tubulin in the MT interior. Tau is a MT-associated protein that binds both ? and ? tubulin on the MT exterior. Both taxol and tau reduce MT dynamics and promote tubulin polymerization. Tau alone also acts as a buttress to bundle, stiffen, and space MTs. A structural study recently suggested that taxol and tau may interact by binding to the same site. Using fluorescence recovery after photobleaching, we find that tau induces taxol to bind MTs cooperatively depending on the tau concentration. We develop a model that correctly fits the data in the absence of tau and yields a measure of taxol cooperativity when tau is present.

  20. Glial Tau Pathology in Tauopathies: Functional Consequences

    PubMed Central

    Kahlson, Martha A.; Colodner, Kenneth J.

    2015-01-01

    Tauopathies are a class of neurodegenerative diseases characterized by the presence of hyperphosphorylated and aggregated tau pathology in neuronal and glial cells. Though the ratio of neuronal and glial tau aggregates varies across diseases, glial tau aggregates can populate the same degenerating brain regions as neuronal tau aggregates. While much is known about the deleterious consequences of tau pathology in neurons, the relative contribution of glial tau pathology to these diseases is less clear. Recent studies using a number of model systems implicate glial tau pathology in contributing to tauopathy pathogenesis. This review aims to highlight the functional consequences of tau overexpression in glial cells and explore the potential contribution of glial tau pathology in the pathogenesis of neurodegenerative tauopathies. PMID:26884683

  1. Lessons from Tau-Deficient Mice

    PubMed Central

    Ke, Yazi D.; Suchowerska, Alexandra K.; van der Hoven, Julia; De Silva, Dineeka M.; Wu, Christopher W.; van Eersel, Janet; Ittner, Arne; Ittner, Lars M.

    2012-01-01

    Both Alzheimer's disease (AD) and frontotemporal dementia (FTD) are characterized by the deposition of hyperphosphorylated forms of the microtubule-associated protein tau in neurons and/or glia. This unifying pathology led to the umbrella term tauopathies for these conditions, also emphasizing the central role of tau in AD and FTD. Generation of transgenic mouse models expressing human tau in the brain has contributed to the understanding of the pathomechanistic role of tau in disease. To reveal the physiological functions of tau in vivo, several knockout mouse strains with deletion of the tau-encoding MAPT gene have been established over the past decade, using different gene targeting constructs. Surprisingly, when initially introduced tau knockout mice presented with no overt phenotype or malformations. The number of publications using tau knockout mice has recently markedly increased, and both behavioural changes and motor deficits have been identified in aged mice of certain strains. Moreover, tau knockout mice have been instrumental in identifying novel functions of tau, both in cultured neurons and in vivo. Importantly, tau knockout mice have significantly contributed to the understanding of the pathophysiological interplay between A? and tau in AD. Here, we review the literature that involves tau knockout mice to summarize what we have learned so far from depleting tau in vivo. PMID:22720190

  2. Insulin dysfunction and Tau pathology

    PubMed Central

    El Khoury, Noura B.; Gratuze, Maud; Papon, Marie-Amélie; Bretteville, Alexis; Planel, Emmanuel

    2013-01-01

    The neuropathological hallmarks of Alzheimer's disease (AD) include senile plaques of β-amyloid (Aβ) peptides (a cleavage product of the Amyloid Precursor Protein, or APP) and neurofibrillary tangles (NFT) of hyperphosphorylated Tau protein assembled in paired helical filaments (PHF). NFT pathology is important since it correlates with the degree of cognitive impairment in AD. Only a small proportion of AD is due to genetic variants, whereas the large majority of cases (~99%) is late onset and sporadic in origin. The cause of sporadic AD is likely to be multifactorial, with external factors interacting with biological or genetic susceptibilities to accelerate the manifestation of the disease. Insulin dysfunction, manifested by diabetes mellitus (DM) might be such factor, as there is extensive data from epidemiological studies suggesting that DM is associated with an increased relative risk for AD. Type 1 diabetes (T1DM) and type 2 diabetes (T2DM) are known to affect multiple cognitive functions in patients. In this context, understanding the effects of diabetes on Tau pathogenesis is important since Tau pathology show a strong relationship to dementia in AD, and to memory loss in normal aging and mild cognitive impairment. Here, we reviewed preclinical studies that link insulin dysfunction to Tau protein pathogenesis, one of the major pathological hallmarks of AD. We found more than 30 studies reporting Tau phosphorylation in a mouse or rat model of insulin dysfunction. We also payed attention to potential sources of artifacts, such as hypothermia and anesthesia, that were demonstrated to results in Tau hyperphosphorylation and could major confounding experimental factors. We found that very few studies reported the temperature of the animals, and only a handful did not use anesthesia. Overall, most published studies showed that insulin dysfunction can promote Tau hyperphosphorylation and pathology, both directly and indirectly, through hypothermia. PMID:24574966

  3. Correlation between flavor-violating decay of long-lived slepton and tau in the coannihilation scenario with the seesaw mechanism

    SciTech Connect

    Kaneko, Satoru; Saito, Hiroki; Sato, Joe; Shimomura, Takashi; Vives, Oscar; Yamanaka, Masato

    2011-06-01

    We investigate flavor violating decays of the long-lived lightest slepton and the tau lepton in the coannihilation region of the minimal supersymmetric standard model with a seesaw mechanism to generate neutrino masses. We consider a situation where the mass difference between the lightest neutralino, as the lightest supersymmetric particle, and the lightest slepton, as the next-to-lightest supersymmetric particle, is smaller than the mass of tau lepton. In this situation, the lifetime of the lightest slepton is very long and it is determined by lepton flavor violating (LFV) couplings because the slepton mainly consists of the lighter stau and the flavor conserving 2-body decay is kinematically forbidden. We show that the lifetime can change many orders of magnitude by varying the Yukawa couplings entering the seesaw mechanism. We also show that the branching ratios of LFV tau decays are strongly correlated with the lightest slepton lifetime. Therefore the branching ratios of LFV tau decays can be determined or constrained by measuring the slepton lifetime at the LHC experiment.

  4. Search for pair production of scalar top quarks decaying to a tau lepton and a b quark in 1.96 TeV ppbar collisions

    SciTech Connect

    Khotilovich, Vadim, G.; /Texas A-M

    2008-05-01

    I present the results of a search for pair production of scalar top quarks ({tilde t}{sub 1}) in an R-parity violating supersymmetric scenario using 322 pb{sup -1} of p{bar p} collisions at {radical}s = 1.96 TeV collected by the upgraded Collider Detector at Fermilab. I assume each {tilde t}{sub 1} decays into a {tau} lepton and a b quark, with branching ratio {beta}, and search for final states containing either an electron or a muon from a leptonic {tau} decay, a hadronically decaying {tau} lepton, and two or more jets. Two candidate events pass my final selection criteria, consistent with the expectation from standard model processes. I present upper limits on the cross section times branching ratio squared {sigma}({tilde t}{sub 1}{bar {tilde t}}{sub 1}) x {beta}{sup 2} as a function of the stop mass m({tilde t}{sub 1}). Assuming {beta} = 1, I set a 95% confidence level limit m({tilde t}{sub 1}) > 153 GeV=c{sup 2}. These limits are also fully applicable to the case of a pair produced third generation scalar leptoquark that decays into a {tau} lepton and a b quark.

  5. Tau in Alzheimer Disease and Related Tauopathies

    PubMed Central

    Iqbal, Khalid; Liu, Fei; Gong, Cheng-Xin; Grundke-Iqbal, Inge

    2011-01-01

    Tau is the major microtubule associated protein (MAP) of a mature neuron. The other two neuronal MAPs are MAP1 and MAP2. An established function of MAPs is their interaction with tubulin and promotion of its assembly into microtubules and stabilization of the microtubule network. The microtubule assembly promoting activity of tau, a phosphoprotein, is regulated by its degree of phosphorylation. Normal adult human brain tau contains 23 moles phosphate/mole of tau protein. Hyperphosphorylation of tau depresses this biological activity of tau. In Alzheimer disease (AD) brain tau is ?three to four-fold more hyperphosphorylated than the normal adult brain tau and in this hyperphosphorylated state it is polymerized into paired helical filaments ([PHF) admixed with straight filaments (SF) forming neurofibrillary tangles. Tau is transiently hyperphosphorylated during development and during anesthesia and hypothermia but not to the same state as in AD brain. The abnormally hyperphosphorylated tau in AD brain is distinguished from transiently hyperphosphorylated tau by its ability (1) to sequester normal tau, MAP1 and MAP2 and disrupt microtubules, and (2) to self-assemble into PHF/SF. The cytosolic abnormally hyperphosphorylated tau, because of oligomerization, unlike normal tau, is sedimentable and on self-assembly into PHF/SF, loses its ability to sequester normal MAPs. Some of the tau in AD brain is truncated which also promotes its self-assembly. Tau mutations found in frontotemporal dementia apparently promote its abnormal hyperphosphorylation. Thus, the AD abnormally hyperphosphorylated tau (1) is distinguishable from both normal and transiently hyperphosphorylated taus, and (2) is inhibitory when in a cytosolic/oligomeric state but not when it is self-assembled into PHF/SF. Inhibition of abnormal hyperphosphorylation of tau offers a promising therapeutic target for AD and related tauopathies. PMID:20678074

  6. The dipion mass spectrum in e+e- annihilation and tau decay: Isospin symmetry breaking effects from the (rho, omega, phi) mixing

    SciTech Connect

    Benayoun, M.; David, P.; Del Buono, L.; Leitner, O.; O'Connell, H.B.; /Fermilab

    2008-01-01

    A way to explain the puzzling difference between the pion form factor as measured in e{sup +}e{sup -} annihilations and in {tau} decays is discussed. We show that isospin symmetry breaking, beside the already identified effects, produces also a full mixing between the {rho}{sup 0}, {omega} and {phi} mesons which generates an isospin 0 component inside the {rho}{sup 0} meson. This effect, not accounted for in current treatments of the problem, seems able to account for the apparent mismatch between e{sup +}e{sup -} and {tau} data below the {phi} mass.

  7. A study of the measurement precision of the Higgs boson decaying into tau pairs at the ILC

    NASA Astrophysics Data System (ADS)

    Kawada, Shin-ichi; Fujii, Keisuke; Suehara, Taikan; Takahashi, Tohru; Tanabe, Tomohiko

    2015-12-01

    We evaluate the measurement precision of the production cross section times the branching ratio of the Higgs boson decaying into tau lepton pairs at the International Linear Collider (ILC). We analyze various final states associated with the main production mechanisms of the Higgs boson, the Higgs-strahlung and WW-fusion processes. The statistical precision of the production cross section times the branching ratio is estimated to be 2.6 and 6.9 % for the Higgs-strahlung and WW-fusion processes, respectively, with the nominal integrated luminosities assumed in the ILC Technical Design Report; the precision improves to 1.0 and 3.4 % with the running scenario including possible luminosity upgrades. The study provides a reference performance of the ILC for future phenomenological analyses.

  8. Updated measurement of the tau lifetime at SLD

    SciTech Connect

    1996-07-23

    We present an updated measurement of the tau lifetime at SLD. 4316 {tau}-pair events, selected from a 150k Z{sup 0} data sample, are analyzed using three techniques: decay length, impact parameter, and impact parameter difference methods. The measurement benefits from the small and stable interaction region at the SLC and the precision CCD pixel vertex detector of the SLD. The combined result is: {tau}{sub {tau}} = 288.1 {+-} 6.1(stat) {+-} 3.3(syst) fs.

  9. From tangles to tau protein.

    PubMed

    Iqbal, K; Novak, M

    2006-01-01

    Alois Alzheimer couldn't have chosen a name more appropriate than neurofibrillary tangles when one hundred years ago (Alzheimer, 1906) he presented this histopathological hallmark of the progressive dementing disorder, which got named after him as Alzheimer disease. Both, the structure and as well as the molecular composition of neurofibrillary tangles have baffled neuroscientists for many years. It was not till 1963 when with the help of the electron microscope the tangles were found to be made up of paired helical filaments (PHF). It took another 23 years before microtubule associated protein tau was immunohistochemically identified as the part of neurofibrillary tangles (Grundke-lqbal, 1986 a). The same year it was shown that tau protein in Alzheimer disease brain was abnormally hyperphosphorylated (Grundke-Iqbal, 1986 b). In 1988 Michal Novak, Cesar Milstein and Claude Wischik produced monoclonal antibody that was able to recognize then unknown protein in PHF. The antibody (MN423) allowed its isolation and let to full molecular characterization as protein tau. These studies provided molecular proof that tau protein was the major and an integral component of the PHF (Wischik et al, 1988 a, b, Goedert et al, 1988, Novak et al, 1989, 1991). Over the years the significance of tau pathology for the neurodegenerative diseases was discussed and often questioned. However, detailed studies of the maturation and distribution of NFTs, showing correlation with degree of cognitive decline and memory impairment in Alzheimer's disease (Braak and Braak, 1991), together with discovery of tau gene mutations causing fronto-temporal dementia in many families (Hutton et al, 1998) promoted tau as the major pathogenic force in neurodegenerative cascade. Further studies focused on tau dysfunctions revealed truncation and phosphorylation as two major posttranslational modifications responsible for toxic gain of function as an underlying cause of tauopathies including Alzheimer's disease (Alonso et al, 1996, Novak et al, 1989, 1991, 1993, Avila et al, 2006). Recently, in vivo experiments using transgenic expression of conformationally modified truncated tau showed that truncation is able to drive neurofibrillary pathology ofAlzheimer's type (Zilka et al, 2006). Finally, after one hundred years the exact nature of the neurofibrillary tangles and their role in neurodegeneration is beginning to be unraveled. PMID:17262984

  10. Search for neutral minimal supersymmetric standard model Higgs bosons decaying to tau pairs in pp collisions at ?s=7 TeV.

    PubMed

    Chatrchyan, S; Khachatryan, V; Sirunyan, A M; Tumasyan, A; Adam, W; Bergauer, T; Dragicevic, M; Er, J; Fabjan, C; Friedl, M; Frhwirth, R; Ghete, V M; Hammer, J; Hnsel, S; Hoch, M; Hrmann, N; Hrubec, J; Jeitler, M; Kasieczka, G; Kiesenhofer, W; Krammer, M; Liko, D; Mikulec, I; Pernicka, M; Rohringer, H; Schfbeck, R; Strauss, J; Teischinger, F; Wagner, P; Waltenberger, W; Walzel, G; Widl, E; Wulz, C-E; Mossolov, V; Shumeiko, N; Suarez Gonzalez, J; Benucci, L; De Wolf, E A; Janssen, X; Maes, T; Mucibello, L; Ochesanu, S; Roland, B; Rougny, R; Selvaggi, M; Van Haevermaet, H; Van Mechelen, P; Van Remortel, N; Blekman, F; Blyweert, S; D'Hondt, J; Devroede, O; Gonzalez Suarez, R; Kalogeropoulos, A; Maes, J; Maes, M; Van Doninck, W; Van Mulders, P; Van Onsem, G P; Villella, I; Charaf, O; Clerbaux, B; De Lentdecker, G; Dero, V; Gay, A P R; Hammad, G H; Hreus, T; Marage, P E; Thomas, L; Vander Velde, C; Vanlaer, P; Adler, V; Cimmino, A; Costantini, S; Grunewald, M; Klein, B; Lellouch, J; Marinov, A; McCartin, J; Ryckbosch, D; Thyssen, F; Tytgat, M; Vanelderen, L; Verwilligen, P; Walsh, S; Zaganidis, N; Basegmez, S; Bruno, G; Caudron, J; Ceard, L; Cortina Gil, E; De Favereau De Jeneret, J; Delaere, C; Favart, D; Giammanco, A; Grgoire, G; Hollar, J; Lemaitre, V; Liao, J; Militaru, O; Ovyn, S; Pagano, D; Pin, A; Piotrzkowski, K; Schul, N; Beliy, N; Caebergs, T; Daubie, E; Alves, G A; Damiao, D De Jesus; Pol, M E; Souza, M H G; Carvalho, W; Da Costa, E M; Martins, C De Oliveira; De Souza, S Fonseca; Mundim, L; Nogima, H; Oguri, V; Da Silva, W L Prado; Santoro, A; Do Amaral, S M Silva; Sznajder, A; De Araujo, F Torres Da Silva; Dias, F A; Tomei, T R Fernandez Perez; Gregores, E M; Lagana, C; Marinho, F; Mercadante, P G; Novaes, S F; Padula, Sandra S; Darmenov, N; Dimitrov, L; Genchev, V; Iaydjiev, P; Piperov, S; Rodozov, M; Stoykova, S; Sultanov, G; Tcholakov, V; Trayanov, R; Vankov, I; Dimitrov, A; Hadjiiska, R; Karadzhinova, A; Kozhuharov, V; Litov, L; Mateev, M; Pavlov, B; Petkov, P; Bian, J G; Chen, G M; Chen, H S; Jiang, C H; Liang, D; Liang, S; Meng, X; Tao, J; Wang, J; Wang, J; Wang, X; Wang, Z; Xiao, H; Xu, M; Zang, J; Zhang, Z; Ban, Y; Guo, S; Guo, Y; Li, W; Mao, Y; Qian, S J; Teng, H; Zhang, L; Zhu, B; Zou, W; Cabrera, A; Moreno, B Gomez; Rios, A A Ocampo; Oliveros, A F Osorio; Sanabria, J C; Godinovic, N; Lelas, D; Lelas, K; Plestina, R; Polic, D; Puljak, I; Antunovic, Z; Dzelalija, M; Brigljevic, V; Duric, S; Kadija, K; Morovic, S; Attikis, A; Galanti, M; Mousa, J; Nicolaou, C; Ptochos, F; Razis, P A; Finger, M; Finger, M; Assran, Y; Khalil, S; Mahmoud, M A; Hektor, A; Kadastik, M; Mntel, M; Raidal, M; Rebane, L; Azzolini, V; Eerola, P; Fedi, G; Czellar, S; Hrknen, J; Heikkinen, A; Karimki, V; Kinnunen, R; Kortelainen, M J; Lampn, T; Lassila-Perini, K; Lehti, S; Lindn, T; Luukka, P; Menp, T; Tuominen, E; Tuominiemi, J; Tuovinen, E; Ungaro, D; Wendland, L; Banzuzi, K; Korpela, A; Tuuva, T; Sillou, D; Besancon, M; Choudhury, S; Dejardin, M; Denegri, D; Fabbro, B; Faure, J L; Ferri, F; Ganjour, S; Gentit, F X; Givernaud, A; Gras, P; de Monchenault, G Hamel; Jarry, P; Locci, E; Malcles, J; Marionneau, M; Millischer, L; Rander, J; Rosowsky, A; Shreyber, I; Titov, M; Verrecchia, P; Baffioni, S; Beaudette, F; Benhabib, L; Bianchini, L; Bluj, M; Broutin, C; Busson, P; Charlot, C; Dahms, T; Dobrzynski, L; Elgammal, S; de Cassagnac, R Granier; Haguenauer, M; Min, P; Mironov, C; Ochando, C; Paganini, P; Sabes, D; Salerno, R; Sirois, Y; Thiebaux, C; Wyslouch, B; Zabi, A; Agram, J-L; Andrea, J; Bloch, D; Bodin, D; Brom, J-M; Cardaci, M; Chabert, E C; Collard, C; Conte, E; Drouhin, F; Ferro, C; Fontaine, J-C; Gel, D; Goerlach, U; Greder, S; Juillot, P; Karim, M; Le Bihan, A-C; Mikami, Y; Van Hove, P; Fassi, F; Mercier, D; Baty, C; Beauceron, S; Beaupere, N; Bedjidian, M; Bondu, O; Boudoul, G; Boumediene, D; Brun, H; Chierici, R; Contardo, D; Depasse, P; El Mamouni, H; Fay, J; Gascon, S; Ille, B; Kurca, T; Le Grand, T; Lethuillier, M; Mirabito, L; Perries, S; Sordini, V; Tosi, S; Tschudi, Y; Verdier, P; Lomidze, D; Anagnostou, G; Edelhoff, M; Feld, L; Heracleous, N; Hindrichs, O; Jussen, R; Klein, K; Merz, J; Mohr, N; Ostapchuk, A; Perieanu, A; Raupach, F; Sammet, J; Schael, S; Sprenger, D; Weber, H; Weber, M; Wittmer, B; Ata, M; Bender, W; Dietz-Laursonn, E; Erdmann, M; Frangenheim, J; Hebbeker, T; Hinzmann, A; Hoepfner, K; Klimkovich, T; Klingebiel, D; Kreuzer, P; Lanske, D; Magass, C; Merschmeyer, M; Meyer, A; Papacz, P; Pieta, H; Reithler, H; Schmitz, S A; Sonnenschein, L; Steggemann, J; Teyssier, D; Tonutti, M; Bontenackels, M; Davids, M; Duda, M; Flgge, G; Geenen, H; Giffels, M; Ahmad, W Haj; Heydhausen, D; Kress, T; Kuessel, Y; Linn, A; Nowack, A; Perchalla, L; Pooth, O; Rennefeld, J; Sauerland, P; Stahl, A; Thomas, M; Tornier, D; Zoeller, M H

    2011-06-10

    A search for neutral minimal supersymmetric standard model (MSSM) Higgs bosons in pp collisions at the LHC at a center-of-mass energy of 7 TeV is presented. The results are based on a data sample corresponding to an integrated luminosity of 36??pb(-1) recorded by the CMS experiment. The search uses decays of the Higgs bosons to tau pairs. No excess is observed in the tau-pair invariant-mass spectrum. The resulting upper limits on the Higgs boson production cross section times branching fraction to tau pairs, as a function of the pseudoscalar Higgs boson mass, yield stringent new bounds in the MSSM parameter space. PMID:21770497

  11. Importance of precision measurements in the tau sector

    SciTech Connect

    Pich, A.

    1996-01-01

    {tau} decays provide a powerful tool to test the structure of the weak currents and the universality of their couplings to the {ital W} boson. The constraints implied by present data and the possible improvements at the {tau}cF are analyzed. {copyright} {ital 1996 American Institute of Physics.}

  12. Determination of the branching ratio tau. -->. rho nu

    SciTech Connect

    Becker, J.J.; Blaylock, G.T.; Bolton, T.; Brown, J.S.; Bunnell, K.O.; Burnett, T.H.; Cassell, R.E.; Coffman, D.; Cook, V.; Coward, D.H.

    1987-02-01

    The decay tau ..-->.. rho nu was studied in tau- pair production by e/sup +/e/sup -/ annihilation at ..sqrt..s = 3.77 GeV. The branching ratio was measured to be B(rho nu) = 22.3 +- 1.4 +- 1.6%. 5 refs., 2 figs.

  13. First measurement of sigma (p anti-p ---> Z) . Br (Z ---> tau tau) at s**(1/2) = 1.96- TeV

    SciTech Connect

    Abazov, V.M.; Abbott, B.; Abolins, M.; Acharya, B.S.; Adams, M.; Adams, T.; Agelou, M.; Agram, J.-L.; Ahn, S.H.; Ahsan, M.; Alexeev, G.D.; Alkhazov, G.; Alton, A.; Alverson, G.; Alves, G.A.; Anastasoaie, M.; Andeen, T.; Anderson, S.; Andrieu, B.; Arnoud, Y.; Askew, A.; /Buenos Aires U. /Rio de Janeiro, CBPF /Rio de Janeiro State U. /Sao Paulo, IFT /Alberta U. /Simon Fraser U. /York U., Canada /McGill U. /Beijing, Inst. High Energy Phys. /Andes U., Bogota /Charles U. /Prague, Tech. U. /Prague, Inst. Phys. /San Francisco de Quito U. /Clermont-Ferrand U. /LPSC, Grenoble /Marseille, CPPM /Orsay, LAL /Paris U., VI-VII /DAPNIA, Saclay /Strasbourg, IReS

    2004-12-01

    The authors present a measurement of the cross section for Z production times the branching fraction to {tau} leptons, {sigma} {center_dot} Br(Z {yields} {tau}{sup +}{tau}{sup -}), in p{bar p} collisions at {radical}s = 1.96 TeV in the channel in which one {tau} decays into {mu}{nu}{sub {mu}}{nu}{sub {tau}}, and the other into hadrons + {nu}{sub {tau}} or e{nu}{sub e}{nu}{sub {tau}}. The data sample corresponds to an integrated luminosity of 226 pb{sup -1} collected with the D0 detector at the Fermilab Tevatron collider. The final sample contains 2008 candidate events with an estimated background of 55%. From this they obtain {sigma} {center_dot} Br(Z {yields} {tau}{sup +}{tau}{sup -}) = 237 {+-} 15(stat) {+-} 18(sys) {+-} 15(lum) pb, in agreement with the standard model prediction.

  14. Usp14 Deficiency Increases Tau Phosphorylation without Altering Tau Degradation or Causing Tau-Dependent Deficits

    PubMed Central

    Jin, Youngnam N.; Chen, Ping-Chung; Watson, Jennifer A.; Walters, Brandon J.; Phillips, Scott E.; Green, Karen; Schmidt, Robert; Wilson, Julie A.; Johnson, Gail V.; Roberson, Erik D.; Dobrunz, Lynn E.; Wilson, Scott M.

    2012-01-01

    Regulated protein degradation by the proteasome plays an essential role in the enhancement and suppression of signaling pathways in the nervous system. Proteasome-associated factors are pivotal in ensuring appropriate protein degradation, and we have previously demonstrated that alterations in one of these factors, the proteasomal deubiquitinating enzyme ubiquitin-specific protease 14 (Usp14), can lead to proteasome dysfunction and neurological disease. Recent studies in cell culture have shown that Usp14 can also stabilize the expression of over-expressed, disease-associated proteins such as tau and ataxin-3. Using Usp14-deficient axJ mice, we investigated if loss of Usp14 results in decreased levels of endogenous tau and ataxin-3 in the nervous system of mice. Although loss of Usp14 did not alter the overall neuronal levels of tau and ataxin-3, we found increased levels of phosphorylated tau that correlated with the onset of axonal varicosities in the Usp14-deficient mice. These changes in tau phosphorylation were accompanied by increased levels of activated phospho-Akt, phosphorylated MAPKs, and inactivated phospho-GSK3β. However, genetic ablation of tau did not alter any of the neurological deficits in the Usp14-deficient mice, demonstrating that increased levels of phosphorylated tau do not necessarily lead to neurological disease. Due to the widespread activation of intracellular signaling pathways induced by the loss of Usp14, a better understanding of the cellular pathways regulated by the proteasome is required before effective proteasomal-based therapies can be used to treat chronic neurological diseases. PMID:23144711

  15. Tau trigger, reconstruction and identification at CMS

    NASA Astrophysics Data System (ADS)

    Calabria, Cesare

    2014-08-01

    The importance of tau leptons in new physics searches at the LHC led the CMS collaboration to design a specific algorithm, the Hadron Plus Strip (HPS) algorithm, for the reconstruction and identification of taus decaying hadronically (?had). The HPS algorithm makes use of a particle description of the event to identify hadronic decay modes of ? leptons through the reconstruction of intermediate resonances. It also provides discriminators against potentially large backgrounds from quarks, gluons and light leptons (electrons and muons). Moreover, thanks to the particle event reconstruction avalaible in CMS, a fast online hadronic tau reconstruction can be performed allowing the development of efficient tau trigger selections which allow to perform a broad range of physics analysis. This report describes the ?had reconstruction and identification of the HPS algorithm and its performances, studied in simulated Z ? ?? events and in samples of proton-proton collision data collected during 2011 and 2012 data-taking at ?{ s} = 7 TeV and 8 TeV , respectively. Finally, the performance of the tau trigger selections is presented.

  16. Spectrophotometric study of Zeta Tau

    NASA Astrophysics Data System (ADS)

    Ivanova, N. L.

    An investigation of 10 spectrograms of Zeta Tau (HD 37202) is presented. Equivalent widths, residual intensities, H line halfwidths, radial velocities of the star and the shell, and the electron density and number of atoms on the second level of hydrogen above the 1-sq-cm surface of the star were obtained. A comparison of present results with those obtained in 1964 shows that the mass of the envelope of Zeta Tau increased in 1973, which is evidenced by an increase in emission intensity in H-alpha and H-beta and the intensification of shell absorption lines.

  17. Elevated cerebrospinal fluid tau in Wernicke encephalopathy

    PubMed Central

    Frijlink, Daphne W; Tilanus, Joachim J; Roks, Gerwin

    2012-01-01

    Wernicke encephalopathy (WE) commonly presents with oculomotor abnormalities, gait ataxia and confusion. WE can mimic rapidly progressive dementia syndromes, such as Creutzfeldt-Jakob disease (CJD). Cerebrospinal fluid (CSF) tau is frequently used for diagnosis of several dementia subtypes, predominantly CJD and Alzheimer's disease. The combination of very high CSF tau (tau) and normal phosphorylated tau (p-tau) levels is almost exclusively seen in aggressive diseases, such as CJD. The authors present a case of a woman with WE, caused by chronic insufficient dietary intake, with highly elevated CSF tau and normal p-tau. The clinical symptoms and CSF findings raised the suspicion of CJD. However, shortly after immediate treatment with thiamine the patient clinically improved. At follow-up, 2.5?months later, she had made a good recovery. This case of rapidly progressive dementia illustrates that, even in the case of a highly elevated CSF tau, clinicians should be alert for treatable causes such as WE. PMID:22879004

  18. The. tau. -lepton and its associated neutrino

    SciTech Connect

    Pich, A. )

    1990-10-10

    This paper discusses the {tau}-lepton and the prospects for future improvements. It is shown how a better understanding of the {tau} properties could be used for testing fundamental aspects of the electroweak and strong interactions.

  19. Tau Splicing and the Intricacies of Dementia

    PubMed Central

    Andreadis, Athena

    2011-01-01

    Tau is a microtubule associated protein that fulfills several functions critical for neuronal formation and health. Tau discharges its functions by producing multiple isoforms via regulated alternative splicing. These isoforms modulate tau function in normal brain by altering the domains of the protein, thereby influencing its localization, conformation and post-translational modifications and hence its availability and affinity for microtubules and other ligands. Disturbances in tau expression result in disruption of the neuronal cytoskeleton and formation of tau structures (neurofibrillary tangles) found in brains of dementia sufferers. More specifically, aberrations in tau splicing regulation directly cause several neurodegenerative diseases which lead to dementia. In this review, I present our cumulative knowledge of tau splicing regulation in connection with neurodegeneration and also briefly go over the still-extensive list of questions that are connected to tau (dys)function. PMID:21604267

  20. Characterization of the in vitro phosphorylation of human tau by tau protein kinase II (cdk5/p20) using mass spectrometry.

    PubMed

    Lund, E T; McKenna, R; Evans, D B; Sharma, S K; Mathews, W R

    2001-02-01

    Hyperphosphorylated tau is an integral part of the neurofibrillary tangles that form within neuronal cell bodies, and tau protein kinase II is reported to play a role in the pathogenesis of Alzheimer's disease. Recently, we reported that tau protein kinase II (cdk5/p20)-phosphorylated human tau inhibits microtubule assembly, and tau protein kinase II (cdk5/p20) phosphorylation of microtubule-associated tau results in dissociation of phosphorylated tau from the microtubules and tubulin depolymerization. In the studies reported here, a combination of mass spectrometric techniques was used to study the phosphorylation of human recombinant tau by recombinant tau protein kinase II (cdk5/p20) in vitro. The extent of phosphorylation was determined by measuring the molecular mass of phosphorylated tau using mass spectrometry. Reaction of human recombinant tau with tau protein kinase II (cdk5/p20) resulted in the formation of two major species containing either five or six phosphate groups. The specific amino acid residues phosphorylated were determined by analyzing tryptic peptides by tandem mass spectrometry via either MALDI/TOF post-source decay or by electrospray tandem mass spectrometry. Based on these experiments, we conclude that tau protein kinase II (cdk5/p20) can phosphorylate human tau at Thr(181), Thr(205), Thr(212), Thr(217), Ser(396) and Ser(404). PMID:11181841

  1. Mutated tau binds less avidly to microtubules than wildtype tau in living cells.

    PubMed

    Nagiec, E W; Sampson, K E; Abraham, I

    2001-02-01

    Some forms of genetically inherited dementia, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), are caused by mutations in tau. We have examined several mutations in the microtubule-binding portion of tau for their effect on microtubule binding, cellular distribution and cytoskeletal structure in mammalian cells. Using constructs coding for mutant (P301L and V337M) and wildtype human tau fused to a green fluorescent protein analog (EGFP) we followed the disposition of tau in live cells after transient transfection using confocal microscopy. Most of the tau protein localized to structures that resembled microtubules or microtubule bundles and co-localized with tubulin. At 3 days post-transfection mutant tau proteins showed a higher abundance of free tau in the cytoplasm than did wildtype tau. Cells expressing the P301L mutation showed proportionally more cytoplasmic localization of tau. Confirming these results, fractionated cells with mutant tau had a higher percentage of tau in the cytoplasmic compartment as compared to the cytoskeletal compartment. Cells with wildtype tau had most tau in the cytoskeletal fraction. Because the mutations (V337M, P301L) are associated with genetic tauopathies, these results suggest that a factor in disease etiology of genetic tauopathies and other dementias with altered tau is a greater abundance of tau in the cytoplasm due to decreased binding to microtubules. This increased cytoplasmic presence may be a significant factor in promoting tau aggregation. PMID:11170176

  2. Prospect for measuring the CP phase in the $h\\tau\\tau$ coupling at the LHC

    SciTech Connect

    Askew, Andrew; Jaiswal, Prerit; Okui, Takemichi; Prosper, Harrison B.; Sato, Nobuo

    2015-04-01

    The search for a new source of CP violation is one of the most important endeavors in particle physics. A particularly interesting way to perform this search is to probe the CP phase in the $h\\tau\\tau$ coupling, as the phase is currently completely unconstrained by all existing data. Recently, a novel variable $\\Theta$ was proposed for measuring the CP phase in the $h\\tau\\tau$ coupling through the $\\tau^\\pm \\to \\pi^\\pm \\pi^0 \

  3. Removing endogenous tau does not prevent tau propagation yet reduces its neurotoxicity.

    PubMed

    Wegmann, Susanne; Maury, Eduardo A; Kirk, Molly J; Saqran, Lubna; Roe, Allyson; DeVos, Sarah L; Nicholls, Samantha; Fan, Zhanyun; Takeda, Shuko; Cagsal-Getkin, Ozge; William, Christopher M; Spires-Jones, Tara L; Pitstick, Rose; Carlson, George A; Pooler, Amy M; Hyman, Bradley T

    2015-12-14

    In Alzheimer's disease and tauopathies, tau protein aggregates into neurofibrillary tangles that progressively spread to synaptically connected brain regions. A prion-like mechanism has been suggested: misfolded tau propagating through the brain seeds neurotoxic aggregation of soluble tau in recipient neurons. We use transgenic mice and viral tau expression to test the hypotheses that trans-synaptic tau propagation, aggregation, and toxicity rely on the presence of endogenous soluble tau. Surprisingly, mice expressing human P301Ltau in the entorhinal cortex showed equivalent tau propagation and accumulation in recipient neurons even in the absence of endogenous tau. We then tested whether the lack of endogenous tau protects against misfolded tau aggregation and toxicity, a second prion model paradigm for tau, using P301Ltau-overexpressing mice with severe tangle pathology and neurodegeneration. Crossed onto tau-null background, these mice had similar tangle numbers but were protected against neurotoxicity. Therefore, misfolded tau can propagate across neural systems without requisite templated misfolding, but the absence of endogenous tau markedly blunts toxicity. These results show that tau does not strictly classify as a prion protein. PMID:26538322

  4. Measurement of the Tau- to F1(1285) Pi- Nu/Tau Branching Fraction And a Search for Second-Class Currents in Tau to Eta-Prime(958) Pi- Nu/Tau

    SciTech Connect

    Alwyn, K.E.; /Manchester U.

    2011-12-01

    The {tau}{sup -} {yields} {eta}{pi}{sup -}{pi}+{pi}{sup -}{nu}{tau} decay with the {eta} {yields} {gamma}{gamma} mode is studied using 384 fb{sup -1} of data collected by the BaBar detector. The branching fraction is measured to be (1.60 {+-} 0.05 {+-} 0.11) x 10{sup -4}. It is found that {tau}{sup -} {yields} f1(1285){pi}{sup -}{nu}{tau} {yields} {eta}{pi}{sup -}{pi}+{pi}{sup -}{nu}{tau} is the dominant decay mode with a branching fraction of (1.11 {+-} 0.06 {+-} 0.05) x 10{sup -4}. The first error is statistical and the second systematic. In addition, a 90% confidence level upper limit on the branching fraction of the {tau}{sup -} {yields} {eta}{prime}(958){pi}{sup -}{nu}{tau} decay is measured to be 7.2 x 10{sup -6}. This last decay proceeds through a second-class current and is expected to be forbidden in the limit of isospin symmetry.

  5. Increased misfolding and truncation of tau in APP/PS1/tau transgenic mice compared to mutant tau mice.

    PubMed

    Hraud, Cline; Goufak, Doris; Ando, Kunie; Leroy, Karelle; Suain, Valrie; Yilmaz, Zehra; De Decker, Robert; Authelet, Michle; Laporte, Vincent; Octave, Jean-Nol; Brion, Jean-Pierre

    2014-02-01

    Neurofibrillary degeneration in transgenic models of tauopathies has been observed to be enhanced when these models are crossed with transgenic models developing an A? pathology. The mechanisms leading to this enhanced tau pathology are not well understood. We have performed a detailed analysis of tau misprocessing in a new transgenic mouse model combining APP, PS1 and tau mutations (5xFADTg30 mice) by comparison with littermates expressing only a FTD mutant tau (Tg30 mice). These 5xFADTg30 mice showed a more severe deficient motor phenotype than Tg30 mice and developed with age a dramatically accelerated NFT load in the brain compared to Tg30 mice. Insoluble tau in 5xFADTg30 mice compared to insoluble tau in Tg30 mice showed increased phosphorylation, enhanced misfolding and truncation changes mimicking more closely the post-translational changes characteristic of PHF-tau in Alzheimer's disease. Endogenous wild-type mouse tau was recruited at much higher levels in insoluble tau in 5xFADTg30 than in Tg30 mice. Extracellular amyloid load, A?40 and A?42, ?-CTFs and ?-CTF phosphorylation levels were lower in 5xFADTg30 mice than in 5xFAD mice. Despite this reduction of A?, a significant hippocampal neuronal loss was observed in 5xFADTg30 but not in 5xFAD mice indicating its closer association with increased tau pathology. This 5xFADTg30 model thus mimics more faithfully tau pathology and neuronal loss observed in AD and suggests that additional post-translational changes in tau and self-recruitment of endogenous tau drive the enhanced tau pathology developing in the presence of A? pathology. PMID:24076100

  6. Study of the $\\tau^- to 3h^- 2h^+ \

    SciTech Connect

    Aubert, Bernard; Barate, R.; Boutigny, D.; Couderc, F.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Tisserand, V.; Zghiche, A.; Grauges, E.; Palano, A.; Pappagallo, M.; Pompili, A.; Chen, J.C.; Qi, N.D.; Rong, G.; Wang, P.; Zhu, Y.S.; Eigen, G.; Ofte, I.; Stugu, B. ,

    2005-05-04

    The branching fraction of the {tau}{sup -} {yields} 3h{sup -} 2h{sup +} {nu}{sub {tau}} decay (h = {pi}, K) is measured with the BABAR detector to be (8.56 {+-} 0.05 {+-} 0.42) x 10{sup -4}, where the first error is statistical and the second systematic. The observed structure of this decay is significantly different from the phase space prediction, with the {rho} resonance playing a strong role. The decay {tau}{sup -} {yields} f{sub 1}(1285){pi}{sup -}{nu}{sub {tau}}, with the f{sub 1}(1285) meson decaying to four charged pions, is observed and the branching fraction is measured to be (3.9 {+-} 0.7 {+-} 0.5) x 10{sup -4}.

  7. Evidence for B{sup -{yields}{tau}-{nu}}{sub {tau}}with a semileptonic tagging method

    SciTech Connect

    Hara, K.; Iijima, T.; Hayasaka, K.; Inami, K.; Miyazaki, Y.; Mori, T.; Ohshima, T.; Senyo, K.; Aihara, H.; Aulchenko, V.; Bondar, A.; Eidelman, S.; Gabyshev, N.; Kuzmin, A.; Shwartz, B.; Zhilich, V.; Zyukova, O.; Aushev, T.; Aziz, T.; Mohanty, G. B.

    2010-10-01

    We present a measurement of the decay B{sup -{yields}{tau}-{nu}}{sub {tau}}using a data sample containing 657x10{sup 6} BB pairs collected at the {Upsilon}(4S) resonance with the Belle detector at the KEKB asymmetric-energy e{sup +}e{sup -} collider. A sample of B{sup +}B{sup -} pairs are tagged by reconstructing one B{sup +} meson decaying semileptonically. We detect the B{sup -{yields}{tau}-{nu}}{sub {tau}}candidate in the recoil. We obtain a signal with a significance of 3.6 standard deviations including systematic uncertainties, and measure the branching fraction to be B(B{sup -{yields}{tau}-{nu}}{sub {tau}})=[1.54{sub -0.37}{sup +0.38}(stat){sub -0.31}{sup +0.29}(syst)]x10{sup -4}. This result confirms the evidence for B{sup -{yields}{tau}-{nu}}{sub {tau}}obtained in a previous Belle measurement that used a hadronic B tagging method.

  8. Searches for the Decays B0 to l+- tau-+ and B+ to l+ nu(L=e,mu) using Hadronic Tag Reconstruction

    SciTech Connect

    Aubert, Bernard; Bona, M.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prudent, X.; Tisserand, V.; Zghiche, A.; Garra Tico, J.; Grauges, E.; Lopez, L.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Abrams, G.S.; Battaglia, M.; Brown, David Nathan; Button-Shafer, J.; Cahn, R.N.; ,

    2008-01-30

    We present searches for the leptonic decays B{sup +} {yields} {ell}{sup +}{nu} and the lepton flavor violating decays B{sup 0} {yields} {ell}{sup {+-}}{tau}{sup {-+}}, where {ell} = e, {mu}, with data collected by the BABAR experiment at SLAC. This search demonstrates a novel technique in which we fully reconstruct the accompanying {bar B} in {Upsilon}(4S) {yields} B{bar B} events, and look for a monoenergetic lepton from the signal B decay. The signal yield is extracted from a fit to the signal lepton candidate momentum distribution in the signal B rest frame. Using a data sample of approximately 378 million B{bar B} pairs (342 fb{sup -1}), we find no evidence of signal in any of the decay modes. Branching fraction upper limits of {Beta}(B{sup +} {yields} e{sup +}{nu}) < 5.2 x 10{sup -6}, {Beta}(B{sup +} {yields} {mu}{sup +}{nu}) < 5.6 x 10{sup -6}, {Beta}(B{sup 0} {yields} e{sup +}{tau}{sup -}) < 2.8 x 10{sup -5} and {Beta}(B{sup 0} {yields} {mu}{sup +}{tau}{sup -}) < 2.2 x 10{sup -5}, are obtained at 90% confidence level.

  9. Advances in tau-based drug discovery

    PubMed Central

    Noble, Wendy; Pooler, Amy M.; Hanger, Diane P.

    2011-01-01

    Introduction Tauopathies, including Alzheimer’s disease (AD) and some frontotemporal dementias, are neurodegenerative diseases characterised by pathological lesions comprised of tau protein. There is currently a significant and urgent unmet need for disease-modifying therapies for these conditions and recently attention has turned to tau as a potential target for intervention. Areas covered Increasing evidence has highlighted pathways associated with tau-mediated neurodegeneration as important targets for drug development. Here, the authors review recently published papers in this area and summarise the genetic and pharmacological approaches that have shown efficacy in reducing tau-associated neurodegeneration. These include the use of agents to prevent abnormal tau processing and increase tau clearance, therapies targeting the immune system, and the manipulation of tau pre-mRNA to modify tau isoform expression. Expert opinion Several small molecule tau-based treatments are currently being assessed in clinical trials, the outcomes of which are eagerly awaited. Current evidence suggests that therapies targeting tau are likely, at least in part, to form the basis of an effective and safe treatment for Alzheimer’s disease and related neurodegenerative disorders in which tau deposition is evident. PMID:22003359

  10. A Simple Model to Study Tau Pathology

    PubMed Central

    Houck, Alexander L.; Hernández, Félix; Ávila, Jesús

    2016-01-01

    Tau proteins play a role in the stabilization of microtubules, but in pathological conditions, tauopathies, tau is modified by phosphorylation and can aggregate into aberrant aggregates. These aggregates could be toxic to cells, and different cell models have been used to test for compounds that might prevent these tau modifications. Here, we have used a cell model involving the overexpression of human tau in human embryonic kidney 293 cells. In human embryonic kidney 293 cells expressing tau in a stable manner, we have been able to replicate the phosphorylation of intracellular tau. This intracellular tau increases its own level of phosphorylation and aggregates, likely due to the regulatory effect of some growth factors on specific tau kinases such as GSK3. In these conditions, a change in secreted tau was observed. Reversal of phosphorylation and aggregation of tau was found by the use of lithium, a GSK3 inhibitor. Thus, we propose this as a simple cell model to study tau pathology in nonneuronal cells due to their viability and ease to work with. PMID:26949341

  11. Measurement of the tau lepton mass by the Beijing Spectrometer (BES) Collaboration

    SciTech Connect

    Soderstrom, E.; BES Collaboration

    1992-11-01

    The mass of the {tau} lepton has been measured at the Beijing Electron Positron Collider using the Beijing Spectrometer. A search near threshold for e{sup +}e{sup {minus}} {yields} {tau}{sup +}{tau}{sup {minus}} was performed. Candidate events were identified by requiring that one {tau} decay via {tau} {yields} e{nu}{bar {nu}}, and the other via {tau} {yields} {mu}{nu}{bar {nu}}. The mass value, obtained from a fit to the energy dependence of the {tau}{sup +}{tau}{sup {minus}} cross section, is m{sub {tau}} = 1776.9{sub -0.5}{sup +0.4} {plus_minus} 0.2 MeV.

  12. Search for squark production in events with jets, hadronically decaying tau leptons and missing transverse energy at s**(1/2) = 1.96-TeV

    SciTech Connect

    Abazov, V.M.; Abbott, B.; Abolins, M.; Acharya, B.S.; Adams, M.; Adams, T.; Aguilo, E.; Ahsan, M.; Alexeev, G.D.; Alkhazov, G.; Alton, A.; /Michigan U. /Northeastern U.

    2009-05-01

    A search for supersymmetric partners of quarks is performed in the topology of multijet events accompanied by at least one tau lepton decaying hadronically and large missing transverse energy. Approximately 1 fb-1 of ppbar collision data from the Fermilab Tevatron Collider at a center of mass energy of 1.96 TeV recorded by the D0 detector is analyzed. Results are combined with the previously published D0 inclusive search for squarks and gluinos. No evidence of physics beyond the standard model is found and lower limits on the squark mass up to 410 GeV are derived in the framework of minimal supergravity with tan(beta)=15, A{sub 0}=-2m{sub 0} and mu<0, in the region where decays to tau leptons dominate. Gaugino masses m{sub 1/2} are excluded up to 172 GeV.

  13. Search for Higgs bosons predicted in two-Higgs-doublet models via decays to tau lepton pairs in 1.96 TeV pp collisions.

    PubMed

    Aaltonen, T; Adelman, J; Akimoto, T; Alvarez Gonzlez, B; Amerio, S; Amidei, D; Anastassov, A; Annovi, A; Antos, J; Apollinari, G; Apresyan, A; Arisawa, T; Artikov, A; Ashmanskas, W; Attal, A; Aurisano, A; Azfar, F; Badgett, W; Barbaro-Galtieri, A; Barnes, V E; Barnett, B A; Barria, P; Bartos, P; Bartsch, V; Bauer, G; Beauchemin, P-H; Bedeschi, F; Beecher, D; Behari, S; Bellettini, G; Bellinger, J; Benjamin, D; Beretvas, A; Beringer, J; Bhatti, A; Binkley, M; Bisello, D; Bizjak, I; Blair, R E; Blocker, C; Blumenfeld, B; Bocci, A; Bodek, A; Boisvert, V; Bolla, G; Bortoletto, D; Boudreau, J; Boveia, A; Brau, B; Bridgeman, A; Brigliadori, L; Bromberg, C; Brubaker, E; Budagov, J; Budd, H S; Budd, S; Burke, S; Burkett, K; Busetto, G; Bussey, P; Buzatu, A; Byrum, K L; Cabrera, S; Calancha, C; Campanelli, M; Campbell, M; Canelli, F; Canepa, A; Carls, B; Carlsmith, D; Carosi, R; Carrillo, S; Carron, S; Casal, B; Casarsa, M; Castro, A; Catastini, P; Cauz, D; Cavaliere, V; Cavalli-Sforza, M; Cerri, A; Cerrito, L; Chang, S H; Chen, Y C; Chertok, M; Chiarelli, G; Chlachidze, G; Chlebana, F; Cho, K; Chokheli, D; Chou, J P; Choudalakis, G; Chuang, S H; Chung, K; Chung, W H; Chung, Y S; Chwalek, T; Ciobanu, C I; Ciocci, M A; Clark, A; Clark, D; Compostella, G; Convery, M E; Conway, J; Cordelli, M; Cortiana, G; Cox, C A; Cox, D J; Crescioli, F; Cuenca Almenar, C; Cuevas, J; Culbertson, R; Cully, J C; Dagenhart, D; Datta, M; Davies, T; de Barbaro, P; De Cecco, S; Deisher, A; De Lorenzo, G; Dell'Orso, M; Deluca, C; Demortier, L; Deng, J; Deninno, M; Derwent, P F; Di Canto, A; di Giovanni, G P; Dionisi, C; Di Ruzza, B; Dittmann, J R; D'Onofrio, M; Donati, S; Dong, P; Donini, J; Dorigo, T; Dube, S; Efron, J; Elagin, A; Erbacher, R; Errede, D; Errede, S; Eusebi, R; Fang, H C; Farrington, S; Fedorko, W T; Feild, R G; Feindt, M; Fernandez, J P; Ferrazza, C; Field, R; Flanagan, G; Forrest, R; Frank, M J; Franklin, M; Freeman, J C; Furic, I; Gallinaro, M; Galyardt, J; Garberson, F; Garcia, J E; Garfinkel, A F; Garosi, P; Genser, K; Gerberich, H; Gerdes, D; Gessler, A; Giagu, S; Giakoumopoulou, V; Giannetti, P; Gibson, K; Gimmell, J L; Ginsburg, C M; Giokaris, N; Giordani, M; Giromini, P; Giunta, M; Giurgiu, G; Glagolev, V; Glenzinski, D; Gold, M; Goldschmidt, N; Golossanov, A; Gomez, G; Gomez-Ceballos, G; Goncharov, M; Gonzlez, O; Gorelov, I; Goshaw, A T; Goulianos, K; Gresele, A; Grinstein, S; Grosso-Pilcher, C; Group, R C; Grundler, U; Guimaraes da Costa, J; Gunay-Unalan, Z; Haber, C; Hahn, K; Hahn, S R; Halkiadakis, E; Han, B-Y; Han, J Y; Happacher, F; Hara, K; Hare, D; Hare, M; Harper, S; Harr, R F; Harris, R M; Hartz, M; Hatakeyama, K; Hays, C; Heck, M; Heijboer, A; Heinrich, J; Henderson, C; Herndon, M; Heuser, J; Hewamanage, S; Hidas, D; Hill, C S; Hirschbuehl, D; Hocker, A; Hou, S; Houlden, M; Hsu, S-C; Huffman, B T; Hughes, R E; Husemann, U; Hussein, M; Huston, J; Incandela, J; Introzzi, G; Iori, M; Ivanov, A; James, E; Jang, D; Jayatilaka, B; Jeon, E J; Jha, M K; Jindariani, S; Johnson, W; Jones, M; Joo, K K; Jun, S Y; Jung, J E; Junk, T R; Kamon, T; Kar, D; Karchin, P E; Kato, Y; Kephart, R; Ketchum, W; Keung, J; Khotilovich, V; Kilminster, B; Kim, D H; Kim, H S; Kim, H W; Kim, J E; Kim, M J; Kim, S B; Kim, S H; Kim, Y K; Kimura, N; Kirsch, L; Klimenko, S; Knuteson, B; Ko, B R; Kondo, K; Kong, D J; Konigsberg, J; Korytov, A; Kotwal, A V; Kreps, M; Kroll, J; Krop, D; Krumnack, N; Kruse, M; Krutelyov, V; Kubo, T; Kuhr, T; Kulkarni, N P; Kurata, M; Kwang, S; Laasanen, A T; Lami, S; Lammel, S; Lancaster, M; Lander, R L; Lannon, K; Lath, A; Latino, G; Lazzizzera, I; LeCompte, T; Lee, E; Lee, H S; Lee, S W; Leone, S; Lewis, J D; Lin, C-S; Linacre, J; Lindgren, M; Lipeles, E; Lister, A; Litvintsev, D O; Liu, C; Liu, T; Lockyer, N S; Loginov, A; Loreti, M; Lovas, L; Lucchesi, D; Luci, C; Lueck, J; Lujan, P; Lukens, P; Lungu, G; Lyons, L; Lys, J; Lysak, R; MacQueen, D; Madrak, R; Maeshima, K; Makhoul, K; Maki, T; Maksimovic, P; Malde, S; Malik, S; Manca, G; Manousakis-Katsikakis, A; Margaroli, F; Marino, C; Marino, C P; Martin, A; Martin, V; Martnez, M; Martnez-Ballarn, R; Maruyama, T; Mastrandrea, P; Masubuchi, T; Mathis, M; Mattson, M E; Mazzanti, P; McFarland, K S; McIntyre, P; McNulty, R; Mehta, A; Mehtala, P; Menzione, A; Merkel, P; Mesropian, C; Miao, T; Miladinovic, N; Miller, R; Mills, C; Milnik, M; Mitra, A; Mitselmakher, G; Miyake, H; Moggi, N; Mondragon, M N; Moon, C S; Moore, R; Morello, M J; Morlock, J; Movilla Fernandez, P; Mlmenstdt, J; Mukherjee, A; Muller, Th; Mumford, R; Murat, P; Mussini, M; Nachtman, J; Nagai, Y; Nagano, A; Naganoma, J; Nakamura, K; Nakano, I; Napier, A; Necula, V; Nett, J; Neu, C; Neubauer, M S; Neubauer, S; Nielsen, J; Nodulman, L; Norman, M; Norniella, O; Nurse, E; Oakes, L; Oh, S H; Oh, Y D; Oksuzian, I; Okusawa, T; Orava, R; Osterberg, K; Pagan Griso, S; Pagliarone, C

    2009-11-13

    We present the results of a search for Higgs bosons predicted in two-Higgs-doublet models, in the case where the Higgs bosons decay to tau lepton pairs, using 1.8 fb(-1) of integrated luminosity of pp collisions recorded by the CDF II experiment at the Fermilab Tevatron. Studying the mass distribution in events where one or both tau leptons decay leptonically, no evidence for a Higgs boson signal is observed. The result is used to infer exclusion limits in the two-dimensional space of tanbeta versus m(A) (the ratio of the vacuum expectation values of the two Higgs doublets and the mass of the pseudoscalar boson, respectively). PMID:20365975

  14. Extracellular monomeric tau protein is sufficient to initiate the spread of tau protein pathology.

    PubMed

    Michel, Claire H; Kumar, Satish; Pinotsi, Dorothea; Tunnacliffe, Alan; St George-Hyslop, Peter; Mandelkow, Eckhard; Mandelkow, Eva-Maria; Kaminski, Clemens F; Kaminski Schierle, Gabriele S

    2014-01-10

    Understanding the formation and propagation of aggregates of the Alzheimer disease-associated Tau protein in vivo is vital for the development of therapeutics for this devastating disorder. Using our recently developed live-cell aggregation sensor in neuron-like cells, we demonstrate that different variants of exogenous monomeric Tau, namely full-length Tau (hTau40) and the Tau-derived construct K18 comprising the repeat domain, initially accumulate in endosomal compartments, where they form fibrillar seeds that subsequently induce the aggregation of endogenous Tau. Using superresolution imaging, we confirm that fibrils consisting of endogenous and exogenous Tau are released from cells and demonstrate their potential to spread Tau pathology. Our data indicate a greater pathological risk and potential toxicity than hitherto suspected for extracellular soluble Tau. PMID:24235150

  15. TTBK2: A Tau Protein Kinase beyond Tau Phosphorylation

    PubMed Central

    Liao, Jung-Chi; Yang, T. Tony; Weng, Rueyhung Roc; Kuo, Ching-Te; Chang, Chih-Wei

    2015-01-01

    Tau tubulin kinase 2 (TTBK2) is a kinase known to phosphorylate tau and tubulin. It has recently drawn much attention due to its involvement in multiple important cellular processes. Here, we review the current understanding of TTBK2, including its sequence, structure, binding sites, phosphorylation substrates, and cellular processes involved. TTBK2 possesses a casein kinase 1 (CK1) kinase domain followed by a ~900 amino acid segment, potentially responsible for its localization and substrate recruitment. It is known to bind to CEP164, a centriolar protein, and EB1, a microtubule plus-end tracking protein. In addition to autophosphorylation, known phosphorylation substrates of TTBK2 include tau, tubulin, CEP164, CEP97, and TDP-43, a neurodegeneration-associated protein. Mutations of TTBK2 are associated with spinocerebellar ataxia type 11. In addition, TTBK2 is essential for regulating the growth of axonemal microtubules in ciliogenesis. It also plays roles in resistance of cancer target therapies and in regulating glucose and GABA transport. Reported sites of TTBK2 localization include the centriole/basal body, the midbody, and possibly the mitotic spindles. Together, TTBK2 is a multifunctional kinase involved in important cellular processes and demands augmented efforts in investigating its functions. PMID:25950000

  16. HST/NICMOS Imaging of HL Tau and XZ Tau

    NASA Astrophysics Data System (ADS)

    Cotera, A. S.; Young, E.; Chen, Hua

    1999-09-01

    We have obtained HST/NICMOS images of HL Tau and XZ Tau using Camera 2 with a nominal plate scale of 0.0755+/-0.005 arcsec/pixel. We selected the filter combination F110W, F160W, F187N, F204M and F212N, to investigate the NIR continuum emission, Paalpha and H_2 features within the region. The data was reduced using the NICRED package and software developed by the NICMOS team. We will present the continuum subtracted narrow band images and point-spread-function (PSF) subtracted images at all wavelengths. The images are diffraction limited with a measured FWHM of ~ 0.''11 at 1.104\\micron. At the distance of HL Tau ( ~ 160 pc), this corresponds to an angular resolution of ?18 AU. Therefore, with the PSF subtracted images we will be able to investigate the properties of the proposed dust accretion disk reported at ~ 150 AU by Close et. al. (1997).

  17. TTBK2: a tau protein kinase beyond tau phosphorylation.

    PubMed

    Liao, Jung-Chi; Yang, T Tony; Weng, Rueyhung Roc; Kuo, Ching-Te; Chang, Chih-Wei

    2015-01-01

    Tau tubulin kinase 2 (TTBK2) is a kinase known to phosphorylate tau and tubulin. It has recently drawn much attention due to its involvement in multiple important cellular processes. Here, we review the current understanding of TTBK2, including its sequence, structure, binding sites, phosphorylation substrates, and cellular processes involved. TTBK2 possesses a casein kinase 1 (CK1) kinase domain followed by a ~900 amino acid segment, potentially responsible for its localization and substrate recruitment. It is known to bind to CEP164, a centriolar protein, and EB1, a microtubule plus-end tracking protein. In addition to autophosphorylation, known phosphorylation substrates of TTBK2 include tau, tubulin, CEP164, CEP97, and TDP-43, a neurodegeneration-associated protein. Mutations of TTBK2 are associated with spinocerebellar ataxia type 11. In addition, TTBK2 is essential for regulating the growth of axonemal microtubules in ciliogenesis. It also plays roles in resistance of cancer target therapies and in regulating glucose and GABA transport. Reported sites of TTBK2 localization include the centriole/basal body, the midbody, and possibly the mitotic spindles. Together, TTBK2 is a multifunctional kinase involved in important cellular processes and demands augmented efforts in investigating its functions. PMID:25950000

  18. A DNA damage-activated checkpoint kinase phosphorylates tau and enhances tau-induced neurodegeneration

    PubMed Central

    Iijima-Ando, Kanae; Zhao, LiJuan; Gatt, Anthony; Shenton, Christopher; Iijima, Koichi

    2010-01-01

    Hyperphosphorylation of the microtubule associated protein tau is detected in the brains of individuals with a range of neurodegenerative diseases including Alzheimer's disease (AD). An imbalance in phosphorylation and/or dephosphorylation of tau at disease-related sites has been suggested to initiate the abnormal metabolism and toxicity of tau in disease pathogenesis. However, the mechanisms underlying abnormal phosphorylation of tau in AD are not fully understood. Here, we show that the DNA damage-activated Checkpoint kinase 2 (Chk2) is a novel tau kinase and enhances tau toxicity in a transgenic Drosophila model. Overexpression of Drosophila Chk2 increases tau phosphorylation at Ser262 and enhances tau-induced neurodegeneration in transgenic flies expressing human tau. The non-phosphorylatable Ser262Ala mutation abolishes Chk2-induced enhancement of tau toxicity, suggesting that the Ser262 phosphorylation site is involved in the enhancement of tau toxicity by Chk2. In vitro kinase assays revealed that human Chk2 and a closely related checkpoint kinase 1 (Chk1) directly phosphorylate human tau at Ser262. We also demonstrate that Drosophila Chk2 does not modulate the activity of the fly homolog of microtubule affinity regulating kinase, which has been shown to be a physiological tau Ser262 kinase. Since accumulation of DNA damage has been detected in the brains of AD patients, our results suggest that the DNA damage-activated kinases Chk1 and Chk2 may be involved in tau phosphorylation and toxicity in the pathogenesis of AD. PMID:20159774

  19. Bimolecular Fluorescence Complementation; Lighting-Up Tau-Tau Interaction in Living Cells

    PubMed Central

    Tak, HyeJin; Haque, Md. Mamunul; Kim, Min Jung; Lee, Joo Hyun; Baik, Ja-Hyun; Kim, YoungSoo; Kim, Dong Jin; Grailhe, Regis; Kim, Yun Kyung

    2013-01-01

    Abnormal tau aggregation is a pathological hallmark of many neurodegenerative disorders and it is becoming apparent that soluble tau aggregates play a key role in neurodegeneration and memory impairment. Despite this pathological importance, there is currently no single method that allows monitoring soluble tau species in living cells. In this regard, we developed a cell-based sensor that visualizes tau self-assembly. By introducing bimolecular fluorescence complementation (BiFC) technique to tau, we were able to achieve spatial and temporal resolution of tau-tau interactions in a range of states, from soluble dimers to large aggregates. Under basal conditions, tau-BiFC cells exhibited little fluorescence intensity, implying that the majority of tau molecules exist as monomers. Upon chemically induced tau hyperphosphorylation, BiFC fluorescence greatly increased, indicating an increased level of tau-tau interactions. As an indicator of tau assembly, our BiFC sensor would be a useful tool for investigating tau pathology. PMID:24312574

  20. Rescue from tau-induced neuronal dysfunction produces insoluble tau oligomers

    PubMed Central

    Cowan, Catherine M.; Quraishe, Shmma; Hands, Sarah; Sealey, Megan; Mahajan, Sumeet; Allan, Douglas W.; Mudher, Amritpal

    2015-01-01

    Aggregation of highly phosphorylated tau is a hallmark of Alzheimer’s disease and other tauopathies. Nevertheless, animal models demonstrate that tau-mediated dysfunction/toxicity may not require large tau aggregates but instead may be caused by soluble hyper-phosphorylated tau or by small tau oligomers. Challenging this widely held view, we use multiple techniques to show that insoluble tau oligomers form in conditions where tau-mediated dysfunction is rescued in vivo. This shows that tau oligomers are not necessarily always toxic. Furthermore, their formation correlates with increased tau levels, caused intriguingly, by either pharmacological or genetic inhibition of tau kinase glycogen-synthase-kinase-3beta (GSK-3β). Moreover, contrary to common belief, these tau oligomers were neither highly phosphorylated, and nor did they contain beta-pleated sheet structure. This may explain their lack of toxicity. Our study makes the novel observation that tau also forms non-toxic insoluble oligomers in vivo in addition to toxic oligomers, which have been reported by others. Whether these are inert or actively protective remains to be established. Nevertheless, this has wide implications for emerging therapeutic strategies such as those that target dissolution of tau oligomers as they may be ineffective or even counterproductive unless they act on the relevant toxic oligomeric tau species. PMID:26608845

  1. The lepton flavor violating decay {tau}{sup {+-}} {yields} Micro-Sign {sup {+-}} Micro-Sign {sup {+-}} Micro-Sign {sup Minus-Or-Plus-Sign} at LHCb

    SciTech Connect

    Keune, A.

    2012-09-15

    The possibility of improving the limit on the branching fraction of the lepton flavor violating decay {tau}{sup {+-}} {yields} Micro-Sign {sup {+-}} Micro-Sign {sup {+-}} Micro-Sign {sup Minus-Or-Plus-Sign} at LHCb is discussed. It is shown that a simple, cut-based analysis is sufficient to improve the upper limit on this branching fraction within the lifetime of LHCb.

  2. Determination of the chiral couplings L{sub 10} and C{sub 87} from semileptonic {tau} decays

    SciTech Connect

    Gonzalez-Alonso, Martin; Pich, Antonio; Prades, Joaquim

    2008-12-01

    Using recent precise hadronic {tau}-decay data on the V-A spectral function, and general properties of QCD such as analyticity, the operator product expansion, and chiral perturbation theory, we get accurate values for the QCD chiral order parameters L{sub 10}{sup r}(M{sub {rho}}) and C{sub 87}{sup r}(M{sub {rho}}). These two low-energy constants appear at order p{sup 4} and p{sup 6}, respectively, in the chiral perturbation theory expansion of the V-A correlator. At order p{sup 4} we obtain L{sub 10}{sup r}(M{sub {rho}})=-(5.22{+-}0.06)x10{sup -3}. Including in the analysis the two-loop (order p{sup 6}) contributions, we get L{sub 10}{sup r}(M{sub {rho}})=-(4.06{+-}0.39)x10{sup -3} and C{sub 87}{sup r}(M{sub {rho}})=(4.89{+-}0.19)x10{sup -3} GeV{sup -2}. In the SU(2) chiral effective theory, the corresponding low-energy coupling takes the value l{sub 5}=13.30{+-}0.11 at order p{sup 4}, and l{sub 5}=12.24{+-}0.21 at order p{sup 6}.

  3. Tau Protein Diffuses along the Microtubule Lattice*

    PubMed Central

    Hinrichs, Maike H.; Jalal, Avesta; Brenner, Bernhard; Mandelkow, Eckhard; Kumar, Satish; Scholz, Tim

    2012-01-01

    Current models for the intracellular transport of Tau protein suggest motor protein-dependent co-transport with microtubule fragments and diffusion of Tau in the cytoplasm, whereas Tau is believed to be stationary while bound to microtubules and in equilibrium with free diffusion in the cytosol. Observations that members of the microtubule-dependent kinesin family show Brownian motion along microtubules led us to hypothesize that diffusion along microtubules could also be relevant in the case of Tau. We used single-molecule total internal reflection fluorescence microscopy to probe for diffusion of individual fluorescently labeled Tau molecules along microtubules. This allowed us to avoid the problem that microtubule-dependent diffusion could be masked by excess of labeled Tau in solution that might occur in in vivo overexpression experiments. We found that approximately half of the individually detected Tau molecules moved bidirectionally along microtubules over distances up to several micrometers. Diffusion parameters such as diffusion coefficient, interaction time, and scanned microtubule length did not change with Tau concentration. Tau binding and diffusion along the microtubule lattice, however, were sensitive to ionic strength and pH and drastically reduced upon enzymatic removal of the negatively charged C termini of tubulin. We propose one-dimensional Tau diffusion guided by the microtubule lattice as one possible additional mechanism for Tau distribution. By such one-dimensional microtubule lattice diffusion, Tau could be guided to both microtubule ends, i.e. the sites where Tau is needed during microtubule polymerization, independently of directed motor-dependent transport. This could be important in conditions where active transport along microtubules might be compromised. PMID:23019339

  4. Measurement of the branching fraction for $\\tau\\to\\eta K\

    SciTech Connect

    del Amo Sanchez, P.; Lees, J.P.; Poireau, V.; Prencipe, E.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Martinelli, M.; Palano, A.; Pappagallo, M.; Eigen, G.; Stugu, B.; Sun, L.; Battaglia, M.; Brown, D.N.; Hooberman, B.; Kerth, L.T.; Kolomensky, Yu.G.; Lynch, G.; Osipenkov, I.L.; Tanabe, T.; /UC, Berkeley /Birmingham U. /Ruhr U., Bochum /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UC, Riverside /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /INFN, Ferrara /Ferrara U. /INFN, Ferrara /INFN, Ferrara /Ferrara U. /INFN, Ferrara /Frascati /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /INFN, Genoa /INFN, Genoa /Genoa U. /Indian Inst. Tech., Guwahati /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa State U. /Iowa State U. /Johns Hopkins U. /Paris U., VI-VII /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /INFN, Milan /Milan U. /INFN, Milan /INFN, Milan /Milan U. /Mississippi U. /Montreal U. /INFN, Naples /Naples U. /NIKHEF, Amsterdam /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /INFN, Padua /Padua U. /INFN, Padua /INFN, Padua /Padua U. /Paris U., VI-VII /INFN, Perugia /Perugia U. /INFN, Pisa /Pisa U. /INFN, Pisa /Pisa, Scuola Normale Superiore /INFN, Pisa /Pisa U. /INFN, Pisa /Princeton U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /INFN, Rome /INFN, Rome /Rome U. /Rostock U. /Rutherford /DAPNIA, Saclay /SLAC /South Carolina U. /Southern Methodist U. /Stanford U., Phys. Dept. /SUNY, Albany /Tel Aviv U. /Tennessee U. /Texas U. /Texas U., Dallas /INFN, Turin /Turin U. /INFN, Trieste /Trieste U. /Valencia U. /Victoria U. /Warwick U. /Wisconsin U., Madison

    2011-08-12

    The authors report on analyses of tau lepton decays {tau}{sup -} {yields} {eta}K{sup -}{nu}{sub {tau}} and {tau}{sup -} {yields} {eta}{pi}{sup -}{nu}{sub {tau}}, with {eta} {yields} {pi}{sup +}{pi}{sup -}{pi}{sup 0}, using 470 fb{sup -1} of data from the BABAR experiment at PEP-II, collected at center-of-mass energies at and near the {Upsilon}(4S) resonance. They measure the branching fraction for the {tau}{sup -} {yields} {eta}K{sup -}{nu}{sub {tau}} decay mode, {Beta}({tau}{sup -} {yields} {eta}K{sup -}{nu}{sub {tau}}) = (1.42 {+-} 0.11(stat) {+-} 0.07(syst)) x 10{sup -4}, and report a 95% confidence level upper limit for the second-class current process {tau}{sup -} {yields} {eta}{pi}{sup -}{nu}{sub {tau}}, {Beta}({tau}{sup -} {yields} {eta}{pi}{sup -}{nu}{sub {tau}}) < 9.9 x 10{sup -5}.

  5. LRRK2 Facilitates tau Phosphorylation through Strong Interaction with tau and cdk5.

    PubMed

    Shanley, Mary R; Hawley, Dillon; Leung, Shirley; Zaidi, Nikhat F; Dave, Roshni; Schlosser, Kate A; Bandopadhyay, Rina; Gerber, Scott A; Liu, Min

    2015-08-25

    Leucine-rich repeat kinase 2 (LRRK2) and tau have been identified as risk factors of Parkinson's disease (PD). As LRRK2 is a kinase and tau is hyperphosphorylated in some LRRK2 mutation carriers of PD patients, the obvious hypothesis is that tau could be a substrate of LRRK2. Previous reports that LRRK2 phosphorylates free tau or tubulin-associated tau provide direct support for this proposition. By comparing LRRK2 with cdk5, we show that wild-type LRRK2 and the G2019S mutant phosphorylate free recombinant full-length tau protein with specific activity 480- and 250-fold lower than cdk5, respectively. More strikingly tau binds to wt LRRK2 or the G2019S mutant 140- or 200-fold more strongly than cdk5. The extremely low activity of LRRK2 but strong binding affinity with tau suggests that LRRK2 may facilitate tau phosphorylation as a scaffold protein rather than as a major tau kinase. This hypothesis is further supported by the observation that (i) cdk5 or tau coimmunoprecipitates with endogenous LRRK2 in SH-SY5Y cells, in mouse brain tissue, and in human PBMCs; (ii) knocking down endogenous LRRK2 by its siRNA in SH-SY5Y cells reduces tau phosphorylation at Ser396 and Ser404; (iii) inhibiting LRRK2 kinase activity by its inhibitors has no effect on tau phosphorylation at these two sites; and (iv) overexpressing wt LRRK2, the G2019S mutant, or the D1994A kinase-dead mutant in SH-SY5Y cells has no effect on tau phosphorylation. Our results suggest that LRRK2 facilitates tau phosphorylation indirectly by recruiting tau or cdk5 rather than by directly phosphorylating tau. PMID:26268594

  6. The acetylation of tau inhibits its function and promotes pathological tau aggregation

    PubMed Central

    Cohen, Todd J.; Guo, Jing L.; Hurtado, David E.; Kwong, Linda K.; Mills, Ian P.; Trojanowski, John Q.; Lee, Virginia M. Y.

    2011-01-01

    The microtubule associated protein tau promotes neuronal survival through binding and stabilization of MTs. Phosphorylation regulates tau–microtubule interactions and hyperphosphorylation contributes to the aberrant formation of insoluble tau aggregates in Alzheimer’s disease (AD) and related tauopathies1. However, other pathogenic post-translational tau modifications have not been well characterized. Here we demonstrate that tau acetylation inhibits tau function via impaired tau–microtubule interactions and promotes pathological tau aggregation. Mass spectrometry analysis identified specific lysine residues, including lysine 280 (K280) within the microtubule-binding motif as the major sites of tau acetylation. Immunohistochemical and biochemical studies of brains from tau transgenic mice and patients with AD and related tauopathies showed that acetylated tau pathology is specifically associated with insoluble, Thioflavin-positive tau aggregates. Thus, tau K280 acetylation in our studies was only detected in diseased tissue, suggesting it may have a role in pathological tau transformation. This study suggests that tau K280 acetylation is a potential target for drug discovery and biomarker development for AD and related tauopathies. PMID:21427723

  7. Glycation alter the process of Tau phosphorylation to change Tau isoforms aggregation property.

    PubMed

    Liu, Kefu; Liu, Yutong; Li, Lingyun; Qin, Peibin; Iqbal, Javed; Deng, Yulin; Qing, Hong

    2016-02-01

    The risk of tauopathies depends in part on the levels and modified composition of six Tau isoforms in the human brain. Abnormal phosphorylation of the Tau protein and the shift of the ratio of 3R Tau to 4R Tau are presumed to result in neurofibrillary pathology and neurodegeneration. Glycation has recently been linked to dementia and metabolic syndrome. To determine the contribution of Tau protein glycation and phosphorylation on Tau aggregation propensity, the assembled kinetics were examined in vitro using Thioflavin T fluorescence assays. We found that glycation and phosphorylation have different effects on aggregation propensity in different Tau isoforms. Different Tau proteins play important parts in each tauopathies, but 3R0N, fetal Tau protein, has no effect on tauopathies. Conversely, 4R2N has more modified sites and a higher tendency to aggregate, playing the most important role in 4R tauopathies. Finally, Glycation, which could modulate Tau phosphorylation, may occur before any other modification. It also regulates the 3R to 4R ratio and promotes 4R2N Tau protein aggregation. Decreasing the sites of glycation, as well as shifting other Tau proteins to 3R0N Tau proteins has potential therapeutic implications for tauopathies. PMID:26655600

  8. Tau oligomers as potential targets for early diagnosis of tauopathy.

    PubMed

    Sahara, Naruhiko; Ren, Yan; Ward, Sarah; Binder, Lester I; Suhara, Tetsuya; Higuchi, Makoto

    2014-01-01

    The discovery of tau mutations in frontotemporal dementia has been a key event in neurodegenerative disease research. The rTg4510 mouse line expressing human tau with P301L FTDP-17-tau mutation has been established to understand the role of tau in neurodegeneration. Our histological analyses with tau antibodies and fluorescent tau ligands on rTg4510 mice revealed that tau oligomer formation was distinct from tangle formation. While in vivo imaging of mature tangles is now available, imaging biomarkers for tau oligomers would be useful for clarifying their roles in neurotoxicity and for diagnosing early-stage tau pathology. PMID:24595194

  9. Search for neutral Higgs bosons decaying to tau pairs in p anti-p collisions at s**(1/2) = 1.96-TeV

    SciTech Connect

    Abazov, V.M.; Abbott, B.; Abolins, M.; Acharya, B.S.; Adams, M.; Adams, T.; Agelou, M.; Agram, J.-L.; Ahn, S.H.; Ahsan, M.; Alexeev, G.D.; /Buenos Aires U. /Rio de Janeiro, CBPF /Rio de Janeiro State U. /Sao Paulo, IFT /Alberta U. /Simon Fraser U. /York U., Canada /McGill U. /Beijing, Inst. High Energy Phys. /Hefei, CUST /Andes U., Bogota

    2006-05-01

    A search for the production of neutral Higgs bosons {Phi} decaying into {tau}{sup +}{tau}{sup -} final states in p{bar p} collisions at a center-of-mass energy of 1.96 TeV is presented. The data, corresponding to an integrated luminosity of approximately 325 pb{sup -1}, were collected by the D0 experiment at the Fermilab Tevatron Collider. Since no excess compared to the expectation from standard model processes is found, limits on the production cross section times branching ratio are set. The results are combined with those obtained from the D0 search for {Phi}b({bar b}) {yields} b{bar b}b({bar b}) and are interpreted in the minimal supersymmetric standard model.

  10. A measurement of the tau Michel parameters at SLD

    SciTech Connect

    Quigley, J.

    1997-05-01

    This thesis presents a measurement of the tau Michel parameters. This measurement utilizes the highly polarized SLC electron beam to extract these quantities directly from the measured tau decay spectra using the 1993--95 SLD sample of 4,528 tau pair events. The results are {rho}{sup e} = 0.71 {+-} 0.14 {+-} 0.05, {xi}{sup e} = 1.16 {+-} 0.52 {+-} 0.06, and ({xi}{delta}){sup e} = 0.85 {+-} 0.43 {+-} 0.08 for tau decays to electrons and {rho}{sup {mu}} = 0.54 {+-} 0.28 {sup {minus}} 0.14, {eta}{sup {mu}} = {minus}0.59 {+-} 0.82 {+-} 0.45, {xi}{sup {mu}} = 0.75 {+-} 0.50 {+-} 0.14, and ({xi}{delta}){sup {mu}} = 0.82 {+-} 0.32 {+-} 0.07 for tau decays to muons. Combining all leptonic tau decays gives {rho} = 0.72 {+-} 0.09 {+-} 0.03, {xi} = 1.05 {+-} 0.35 {+-} 0.04, and {Xi}{delta} = 0.88 {+-} 0.27 {+-} 0.04. These results agree well with the current world average and the Standard Model.

  11. Analyzing Tau Aggregation with Electron Microscopy.

    PubMed

    Huseby, Carol J; Kuret, Jeff

    2016-01-01

    Conversion of monomeric tau protein into filamentous aggregates is a defining event in the pathogenesis of Alzheimer's disease. To gain insight into disease pathogenesis, the mechanisms that trigger and mediate tau aggregation are under intense investigation. Characterization efforts have relied primarily on recombinant tau protein preparations and high-throughput solution-based detection methods such as thioflavin-dye fluorescence and laser-light-scattering spectroscopies. Transmission electron microscopy (TEM) is a static imaging tool that complements these approaches by detecting individual tau filaments at nanometer resolution. In doing so, it can provide unique insight into the quality, quantity, and composition of synthetic tau filament populations. Here we describe protocols for analysis of tau filament populations by TEM for purposes of dissecting aggregation mechanism. PMID:26453208

  12. Tau as a biomarker of neurodegenerative diseases

    PubMed Central

    Schraen-Maschke, Susanna; Sergeant, Nicolas; Dhaenens, Claire-Marie; Bombois, Stephanie; Deramecourt, Vincent; Caillet-Boudin, Marie-Laure; Pasquier, Florence; Maurage, Claude-Alain; Sablonniere, Bernard; Vanmechelen, Eugeen; Buee, Luc

    2008-01-01

    Summary The microtubule associated protein Tau is mainly expressed in neurons of the central nervous system and is crucial in axonal maintenance and axonal transport. The rationale for Tau as a biomarker of neurodegenerative diseases is that it is a major component of abnormal intraneuronal aggregates observed in numerous of these diseases named Tauopathies, including Alzheimers disease. The molecular diversity of Tau is very useful when analysing it in the brain or in the peripheral fluids. Immunohistochemical and biochemical characterisation of Tau aggregates in the brain allows the post-mortem classification and differential diagnosis of Tauopathies. As peripheral biomarker of Alzheimers disease in the cerebrospinal fluid, Tau proteins are now validated for diagnosis and predictive purposes. For the future, the detailed characterization of Tau in brain and in peripheral fluids will lead to novel promising biomarkers for differential diagnosis of dementia and monitoring of therapeutics. PMID:20477391

  13. Differential induction and spread of tau pathology in young PS19 tau transgenic mice following intracerebral injections of pathological tau from Alzheimer's disease or corticobasal degeneration brains.

    PubMed

    Boluda, Susana; Iba, Michiyo; Zhang, Bin; Raible, Kevin M; Lee, Virginia M-Y; Trojanowski, John Q

    2015-02-01

    Filamentous tau pathologies are hallmark lesions of several neurodegenerative tauopathies including Alzheimer's disease (AD) and corticobasal degeneration (CBD) which show cell type-specific and topographically distinct tau inclusions. Growing evidence supports templated transmission of tauopathies through functionally interconnected neuroanatomical pathways suggesting that different self-propagating strains of pathological tau could account for the diverse manifestations of neurodegenerative tauopathies. Here, we describe the rapid and distinct cell type-specific spread of pathological tau following intracerebral injections of CBD or AD brain extracts enriched in pathological tau (designated CBD-Tau and AD-Tau, respectively) in young human mutant P301S tau transgenic (Tg) mice (line PS19) ~6-9 months before they show onset of mutant tau transgene-induced tau pathology. At 1 month post-injection of CBD-Tau, tau inclusions developed predominantly in oligodendrocytes of the fimbria and white matter near the injection sites with infrequent intraneuronal tau aggregates. In contrast, injections of AD-Tau in young PS19 mice induced tau pathology predominantly in neuronal perikarya with little or no oligodendrocyte involvement 1 month post-injection. With longer post-injection survival intervals of up to 6 months, CBD-Tau- and AD-Tau-induced tau pathology spread to different brain regions distant from the injection sites while maintaining the cell type-specific pattern noted above. Finally, CA3 neuron loss was detected 3 months post-injection of AD-Tau but not CBD-Tau. Thus, AD-Tau and CBD-Tau represent specific pathological tau strains that spread differentially and may underlie distinct clinical and pathological features of these two tauopathies. Hence, these strains could become targets to develop disease-modifying therapies for CBD and AD. PMID:25534024

  14. Measurement of the tau polarisation at the Z resonance

    NASA Astrophysics Data System (ADS)

    Buskulic, D.; Decamp, D.; Goy, C.; Lees, J.-P.; Minard, M.-N.; Mours, B.; Pietrzyk, B.; Alemany, R.; Ariztizabal, F.; Comas, P.; Crespo, J. M.; Delfino, M.; Fenandez, E.; Fernandez-Bosman, M.; Gaitan, V.; Garrido, Ll.; Mattison, T.; Pacheco, A.; Padilla, C.; Pascual, A.; Creanza, D.; de Palma, M.; Farilla, A.; Iaselli, G.; Maggi, G.; Maggi, M.; Natali, S.; Nuzzo, S.; Quattromini, M.; Ranieri, A.; Raso, G.; Romano, F.; Ruggieri, F.; Selvaggi, G.; Silvestris, L.; Tempesta, P.; Zito, G.; Chai, Y.; Hu, H.; Huang, D.; Huang, X.; Lin, J.; Wang, T.; Xie, Y.; Xu, D.; Xu, R.; Zhang, J.; Zhao, W.; Bauerdick, L. A. T.; Blucher, E.; Bonvicini, G.; Boudreau, J.; Casper, D.; Drevermann, H.; Forty, R. W.; Ganis, G.; Gay, C.; Hagelberg, R.; Harvey, J.; Haywood, S.; Hilgart, J.; Jacobsen, R.; Jost, B.; Knobloch, J.; Lehraus, I.; Lohse, T.; Lusiani, A.; Martinez, M.; Mato, P.; Meinhard, H.; Minten, A.; Miotto, A.; Miquel, R.; Moser, H.-G.; Palazzi, P.; Perlas, J. A.; Pusztaszeri, J.-F.; Ranjard, F.; Redlinger, G.; Rolandi, L.; Rothberg, J.; Ruan, T.; Saich, M.; Schlatter, D.; Schmelling, M.; Sefkow, F.; Tejessy, W.; Wachsmuth, H.; Wiedenmann, W.; Wildish, T.; Witzeling, W.; Wotschack, J.; Ajaltouni, Z.; Badaud, F.; Bardadin-Otwinowska, M.; El Fellous, R.; Falvard, A.; Gay, P.; Guicheney, C.; Henrard, P.; Jousset, J.; Michel, B.; Montret, J.-C.; Pallin, D.; Perret, P.; Podlyski, F.; Proriol, J.; Prulhire, F.; Saadi, F.; Fearnley, T.; Hansen, J. D.; Hansen, J. R.; Hansen, P. H.; Mllerud, R.; Nilsson, B. S.; Candlin, D. J.; Parsons, M. I.; Veitch, E.; Moneta, L.; Parrini, G.; Corden, M.; Georgiopoulos, C.; Ikeda, M.; Lannutti, J.; Levinthal, D.; Mermikides, M.; Sawyer, L.; Wasserbaech, S.; Antonelli, A.; Baldini, R.; Bencivenni, G.; Bologna, G.; Bossi, F.; Campana, P.; Capon, G.; Cerutti, F.; Chiarella, V.; D'Ettorre-Piazzoli, B.; Felici, G.; Laurelli, P.; Mannocchi, G.; Murtas, F.; Murtas, G. P.; Passalacqua, L.; Pepe-Altarelli, M.; Picchi, P.; Colrain, P.; Ten Have, I.; Lynch, J. G.; Maitland, W.; Morton, W. T.; Raine, C.; Reeves, P.; Scarr, J. M.; Smith, K.; Smith, M. G.; Thompson, A. S.; Turnbull, R. M.; Brandl, B.; Braun, O.; Geweniger, C.; Hanke, P.; Hepp, V.; Kluge, E. E.; Maumary, Y.; Putzer, A.; Rensch, B.; Stahl, A.; Tittel, K.; Wunsch, M.; Belk, A. T.; Beuselinck, R.; Binnie, D. M.; Cameron, W.; Cattaneo, M.; Colling, D. J.; Dornan, P. J.; Dugeay, S.; Greene, A. M.; Hassaed, J. F.; Lieske, N. M.; Nash, J.; Payne, D. G.; Phillips, M. J.; Sedgbeer, J. K.; Tomalin, I. R.; Wright, A. G.; Girtler, P.; Kneringer, E.; Kuhn, D.; Rudolph, G.; Bowdery, C. K.; Brodbeck, T. J.; Finch, A. J.; Foster, F.; Hughes, G.; Jackson, D.; Keemer, N. R.; Nuttall, M.; Patel, A.; Sloan, T.; Snow, S. W.; Whelan, E. P.; Efthymiopoulos, I.; Kyriakis, A.; Simopoulou, E.; Vayaki, A.; Zachariadou, K.; Badier, J.; Blondel, A.; Bonneaud, G.; Brient, J. C.; Fouque, G.; Orteu, S.; Roug, A.; Rumpf, M.; Tanaka, R.; Verderi, M.; Videau, H.; Adlung, S.; Assmann, R.; Bauer, C.; Blum, W.; Brown, D.; Cattaneo, P.; Dehning, B.; Dietl, H.; Dydak, F.; Frank, M.; Halley, A. W.; Lauber, J.; Ltjens, G.; Lutz, G.; Mnner, W.; Richter, R.; Rotscheidt, H.; Schrder, J.; Schwarz, A. S.; Settles, R.; Seywerd, H.; Stierlin, U.; Stiegler, U.; Denis, R. St.; Wolf, G.; Boucrot, J.; Callot, O.; Cordier, A.; Davier, M.; Duflot, L.; Grivaz, J.-F.; Heusse, Ph.; Jaffe, D. E.; Janot, P.; Kim, D. W.; Le Diberder, F.; Lefranois, J.; Lutz, A.-M.; Schune, M.-H.; Veillet, J.-J.; Videau, I.; Zhang, Z.; Abbaneo, D.; Bagliesi, G.; Batignani, G.; Bosisio, L.; Bottigli, U.; Bozzi, C.; Calderini, G.; Carpinelli, M.; Ciocci, M. A.; Dell'Orso, R.; Ferrante, I.; Fidecaro, F.; Foa, L.; Focardi, E.; Forti, F.; Giassi, A.; Giorgi, M. A.; Gregorio, A.; Ligabue, F.; Mannelli, E. B.; Marrocchesi, P. S.; Messineo, A.; Palla, F.; Rizzo, G.; Sanguinetti, G.; Spagnolo, P.; Steinberger, J.; Tenchini, R.; Tonelli, G.; Triggiani, G.; Vannini, C.; Venturi, A.; Verdini, P. G.; Walsh, J.; Betteridge, A. P.; Carter, J. M.; Green, M. G.; March, P. V.; Mir, Ll. M.; Medcalf, T.; Quazi, I. S.; Strong, J. A.; West, L. R.; Botterill, D. R.; Clifft, R. W.; Edgecock, T. R.; Edwards, M.; Fisher, S. M.; Jones, T. J.; Norton, P. R.; Salmon, D. P.; Thompson, J. C.; Kleinknecht, K.; Raab, J.; Renk, B.; Sander, H.-G.; Schmidt, H.; Steeg, F.; Walther, S. M.; Wanke, R.; Wolf, B.; Aubert, J.-J.; Bencheikh, A. M.; Benchouk, C.; Bonissent, A.; Carr, J.; Coyle, P.; Drinkard, J.; Etienne, F.; Nicod, D.; Papalexiou, S.; Payre, P.; Roos, L.; Rousseau, D.; Schwemling, P.; Talby, M.; Bloch-Devaux, B.; Colas, P.; Duarte, H.; Kozanecki, W.; Lanon, E.; Lemaire, M. C.; Locci, E.; Perez, P.; Perrier, F.; Rander, J.; Renardy, J.-F.; Rosowsky, A.; Roussarie, A.; Schuller, J.-P.; Schwindling, J.; Si Mohand, D.; Vallage, B.

    1993-09-01

    Using 18.8 pb-1 of data collected in 1990 and 1991, ALEPH has measured the tau polarisation in the decay modes ?? ev bar v, ??? v bar v, ????, ???? and ?? a 1?, using both the individual tau decay kinematics and the event acollinearity. The measurement of the tau polarisation as a function of the production polar angle yields the two parameters A ? and A e , where A l =2 g {/v l } g {/A l }/( g {/v l })2+( g {/A l })2] The results A ?=0.1430.023 and A e =0.1200.026 are consistent with the hypothesis of electron-tau universality. Assuming universality yields a measurement of the effective weak mixing angle sin2?{/w eff}=0.23320.0022.

  15. Searches for violation of lepton flavour and baryon number in tau lepton decays at LHCb

    NASA Astrophysics Data System (ADS)

    Aaij, R.; Abellan Beteta, C.; Adeva, B.; Adinolfi, M.; Adrover, C.; Affolder, A.; Ajaltouni, Z.; Albrecht, J.; Alessio, F.; Alexander, M.; Ali, S.; Alkhazov, G.; Alvarez Cartelle, P.; Alves, A. A.; Amato, S.; Amerio, S.; Amhis, Y.; Anderlini, L.; Anderson, J.; Andreassen, R.; Appleby, R. B.; Aquines Gutierrez, O.; Archilli, F.; Artamonov, A.; Artuso, M.; Aslanides, E.; Auriemma, G.; Bachmann, S.; Back, J. J.; Baesso, C.; Balagura, V.; Baldini, W.; Barlow, R. J.; Barschel, C.; Barsuk, S.; Barter, W.; Bauer, Th.; Bay, A.; Beddow, J.; Bedeschi, F.; Bediaga, I.; Belogurov, S.; Belous, K.; Belyaev, I.; Ben-Haim, E.; Bencivenni, G.; Benson, S.; Benton, J.; Berezhnoy, A.; Bernet, R.; Bettler, M.-O.; van Beuzekom, M.; Bien, A.; Bifani, S.; Bird, T.; Bizzeti, A.; Bjrnstad, P. M.; Blake, T.; Blanc, F.; Blouw, J.; Blusk, S.; Bocci, V.; Bondar, A.; Bondar, N.; Bonivento, W.; Borghi, S.; Borgia, A.; Bowcock, T. J. V.; Bowen, E.; Bozzi, C.; Brambach, T.; van den Brand, J.; Bressieux, J.; Brett, D.; Britsch, M.; Britton, T.; Brook, N. H.; Brown, H.; Burducea, I.; Bursche, A.; Busetto, G.; Buytaert, J.; Cadeddu, S.; Callot, O.; Calvi, M.; Calvo Gomez, M.; Camboni, A.; Campana, P.; Campora Perez, D.; Carbone, A.; Carboni, G.; Cardinale, R.; Cardini, A.; Carranza-Mejia, H.; Carson, L.; Carvalho Akiba, K.; Casse, G.; Castillo Garcia, L.; Cattaneo, M.; Cauet, Ch.; Charles, M.; Charpentier, Ph.; Chen, P.; Chiapolini, N.; Chrzaszcz, M.; Ciba, K.; Cid Vidal, X.; Ciezarek, G.; Clarke, P. E. L.; Clemencic, M.; Cliff, H. V.; Closier, J.; Coca, C.; Coco, V.; Cogan, J.; Cogneras, E.; Collins, P.; Comerma-Montells, A.; Contu, A.; Cook, A.; Coombes, M.; Coquereau, S.; Corti, G.; Couturier, B.; Cowan, G. A.; Craik, D. C.; Cunliffe, S.; Currie, R.; D'Ambrosio, C.; David, P.; David, P. N. Y.; Davis, A.; De Bonis, I.; De Bruyn, K.; De Capua, S.; De Cian, M.; De Miranda, J. M.; De Paula, L.; De Silva, W.; De Simone, P.; Decamp, D.; Deckenhoff, M.; Del Buono, L.; Dlage, N.; Derkach, D.; Deschamps, O.; Dettori, F.; Di Canto, A.; Di Ruscio, F.; Dijkstra, H.; Dogaru, M.; Donleavy, S.; Dordei, F.; Dosil Surez, A.; Dossett, D.; Dovbnya, A.; Dupertuis, F.; Dzhelyadin, R.; Dziurda, A.; Dzyuba, A.; Easo, S.; Egede, U.; Egorychev, V.; Eidelman, S.; van Eijk, D.; Eisenhardt, S.; Eitschberger, U.; Ekelhof, R.; Eklund, L.; El Rifai, I.; Elsasser, Ch.; Elsby, D.; Falabella, A.; Frber, C.; Fardell, G.; Farinelli, C.; Farry, S.; Fave, V.; Ferguson, D.; Fernandez Albor, V.; Ferreira Rodrigues, F.; Ferro-Luzzi, M.; Filippov, S.; Fiore, M.; Fitzpatrick, C.; Fontana, M.; Fontanelli, F.; Forty, R.; Francisco, O.; Frank, M.; Frei, C.; Frosini, M.; Furcas, S.; Furfaro, E.; Gallas Torreira, A.; Galli, D.; Gandelman, M.; Gandini, P.; Gao, Y.; Garofoli, J.; Garosi, P.; Garra Tico, J.; Garrido, L.; Gaspar, C.; Gauld, R.; Gersabeck, E.; Gersabeck, M.; Gershon, T.; Ghez, Ph.; Gibson, V.; Gligorov, V. V.; Gbel, C.; Golubkov, D.; Golutvin, A.; Gomes, A.; Gordon, H.; Grabalosa Gndara, M.; Graciani Diaz, R.; Granado Cardoso, L. A.; Graugs, E.; Graziani, G.; Grecu, A.; Greening, E.; Gregson, S.; Griffith, P.; Grnberg, O.; Gui, B.; Gushchin, E.; Guz, Yu.; Gys, T.; Hadjivasiliou, C.; Haefeli, G.; Haen, C.; Haines, S. C.; Hall, S.; Hampson, T.; Hansmann-Menzemer, S.; Harnew, N.; Harnew, S. T.; Harrison, J.; Hartmann, T.; He, J.; Heijne, V.; Hennessy, K.; Henrard, P.; Hernando Morata, J. A.; van Herwijnen, E.; Hicks, E.; Hill, D.; Hoballah, M.; Hombach, C.; Hopchev, P.; Hulsbergen, W.; Hunt, P.; Huse, T.; Hussain, N.; Hutchcroft, D.; Hynds, D.; Iakovenko, V.; Idzik, M.; Ilten, P.; Jacobsson, R.; Jaeger, A.; Jans, E.; Jaton, P.; Jing, F.; John, M.; Johnson, D.; Jones, C. R.; Joram, C.; Jost, B.; Kaballo, M.; Kandybei, S.; Karacson, M.; Karbach, T. M.; Kenyon, I. R.; Kerzel, U.; Ketel, T.; Keune, A.; Khanji, B.; Kochebina, O.; Komarov, I.; Koopman, R. F.; Koppenburg, P.; Korolev, M.; Kozlinskiy, A.; Kravchuk, L.; Kreplin, K.; Kreps, M.; Krocker, G.; Krokovny, P.; Kruse, F.; Kucharczyk, M.; Kudryavtsev, V.; Kvaratskheliya, T.; La Thi, V. N.; Lacarrere, D.; Lafferty, G.; Lai, A.; Lambert, D.; Lambert, R. W.; Lanciotti, E.; Lanfranchi, G.; Langenbruch, C.; Latham, T.; Lazzeroni, C.; Le Gac, R.; van Leerdam, J.; Lees, J.-P.; Lefvre, R.; Leflat, A.; Lefranois, J.; Leo, S.; Leroy, O.; Lesiak, T.; Leverington, B.; Li, Y.; Li Gioi, L.; Liles, M.; Lindner, R.; Linn, C.; Liu, B.; Liu, G.; Lohn, S.; Longstaff, I.; Lopes, J. H.; Lopez Asamar, E.; Lopez-March, N.; Lu, H.; Lucchesi, D.; Luisier, J.; Luo, H.; Machefert, F.; Machikhiliyan, I. V.; Maciuc, F.; Maev, O.; Malde, S.; Manca, G.; Mancinelli, G.; Marconi, U.; Mrki, R.; Marks, J.; Martellotti, G.; Martens, A.; Martin, L.; Martn Snchez, A.; Martinelli, M.; Martinez Santos, D.; Martins Tostes, D.

    2013-07-01

    Searches for the lepton flavour violating decay ?- ??-?+?- and the lepton flavour and baryon number violating decays ?- ?pbar?+?- and ?- ? p?-?- have been carried out using proton-proton collision data, corresponding to an integrated luminosity of 1.0fb-1, taken by the LHCb experiment at ?{ s} = 7TeV. No evidence has been found for any signal, and limits have been set at 90% confidence level on the branching fractions: B (?- ??-?+?-) < 8.0 10-8, B (?- ?pbar?+?-) < 3.3 10-7 and B (?- ? p?-?-) < 4.4 10-7. The results for the ?- ?pbar?+?- and ?- ? p?-?- decay modes represent the first direct experimental limits on these channels.

  16. Interaction of tau protein with model lipid membranes induces tau structural compaction and membrane disruption

    PubMed Central

    Jones, Emmalee M.; Dubey, Manish; Camp, Phillip J.; Vernon, Briana C.; Biernat, Jacek; Mandelkow, Eckhard; Majewski, Jaroslaw; Chi, Eva Y.

    2012-01-01

    The misfolding and aggregation of the intrinsically disordered, microtubule-associated tau protein into neurofibrillary tangles is implicated in the pathogenesis of Alzheimer's disease. However, the mechanisms of tau aggregation and toxicity remain unknown. Recent work has shown that lipid membrane can induce tau aggregation and that membrane permeabilization may serve as a pathway by which protein aggregates exert toxicity, suggesting that the plasma membrane may play dual roles in tau pathology. This prompted our investigation to assess tau's propensity to interact with membranes and to elucidate the mutually disruptive structural perturbations the interactions induce in both tau and the membrane. We show that although highly charged and soluble, the full-length tau (hTau40) is also highly surface active, selectively inserts into anionic DMPG lipid monolayers and induces membrane morphological changes. To resolve molecular-scale structural details of hTau40 associated with lipid membranes, X-ray and neutron scattering techniques are utilized. X-ray reflectivity indicates hTau40's presence underneath a DMPG monolayer and penetration into the lipid headgroups and tailgroups, whereas grazing incidence X-ray diffraction shows that hTau40 insertion disrupts lipid packing. Moreover, both air/water and DMPG lipid membrane interfaces induce the disordered hTau40 to partially adopt a more compact conformation with density similar to that of a folded protein. Neutron reflectivity shows that tau completely disrupts supported DMPG bilayers while leaving the neutral DPPC bilayer intact. Our results show that hTau40's strong interaction with anionic lipids induces tau structural compaction and membrane disruption, suggesting possible membrane-based mechanisms of tau aggregation and toxicity in neurodegenerative diseases. PMID:22401494

  17. Searching for tau neutrinos with Cherenkov telescopes

    NASA Astrophysics Data System (ADS)

    Gra, D.; Bernardini, E.; Kappes, A.

    2015-02-01

    Cherenkov telescopes have the capability of detecting high energy tau neutrinos in the energy range of 1-1000 PeV by searching for very inclined showers. If a tau lepton, produced by a tau neutrino, escapes from the Earth or a mountain, it will decay and initiate a shower in the air which can be detected by an air shower fluorescence or Cherenkov telescope. In this paper, we present detailed Monte Carlo simulations of corresponding event rates for the VERITAS and two proposed Cherenkov Telescope Array sites: Meteor Crater and Yavapai Ranch, which use representative AGN neutrino flux models and take into account topographic conditions of the detector sites. The calculated neutrino sensitivities depend on the observation time and the shape of the energy spectrum, but in some cases are comparable or even better than corresponding neutrino sensitivities of the IceCube detector. For VERITAS and the considered Cherenkov Telescope Array sites the expected neutrino sensitivities are up to factor 3 higher than for the MAGIC site because of the presence of surrounding mountains.

  18. Measurement of the tau lepton polarisation at LEP2

    NASA Astrophysics Data System (ADS)

    DELPHI Collaboration; Abdallah, J.; Abreu, P.; Adam, W.; Adzic, P.; Albrecht, T.; Alemany-Fernandez, R.; Allmendinger, T.; Allport, P. P.; Amaldi, U.; Amapane, N.; Amato, S.; Anashkin, E.; Andreazza, A.; Andringa, S.; Anjos, N.; Antilogus, P.; Apel, W.-D.; Arnoud, Y.; Ask, S.; Asman, B.; Augustin, J. E.; Augustinus, A.; Baillon, P.; Ballestrero, A.; Bambade, P.; Barbier, R.; Bardin, D.; Barker, G. J.; Baroncelli, A.; Battaglia, M.; Baubillier, M.; Becks, K.-H.; Begalli, M.; Behrmann, A.; Ben-Haim, E.; Benekos, N.; Benvenuti, A.; Berat, C.; Berggren, M.; Bertrand, D.; Besancon, M.; Besson, N.; Bloch, D.; Blom, M.; Bluj, M.; Bonesini, M.; Boonekamp, M.; Booth, P. S. L.; Borisov, G.; Botner, O.; Bouquet, B.; Bowcock, T. J. V.; Boyko, I.; Bracko, M.; Brenner, R.; Brodet, E.; Bruckman, P.; Brunet, J. M.; Buschbeck, B.; Buschmann, P.; Calvi, M.; Camporesi, T.; Canale, V.; Carena, F.; Castro, N.; Cavallo, F.; Chapkin, M.; Charpentier, Ph.; Checchia, P.; Chierici, R.; Chliapnikov, P.; Chudoba, J.; Chung, S. U.; Cieslik, K.; Collins, P.; Contri, R.; Cosme, G.; Cossutti, F.; Costa, M. J.; Crennell, D.; Cuevas, J.; D'Hondt, J.; da Silva, T.; da Silva, W.; Dedovich, D.; Ricca, G. Della; de Angelis, A.; de Boer, W.; de Clercq, C.; de Lotto, B.; de Maria, N.; de Min, A.; de Paula, L.; di Ciaccio, L.; di Simone, A.; Doroba, K.; Drees, J.; Eigen, G.; Ekelof, T.; Ellert, M.; Elsing, M.; Santo, M. C. Espirito; Fanourakis, G.; Fassouliotis, D.; Feindt, M.; Fernandez, J.; Ferrer, A.; Ferro, F.; Flagmeyer, U.; Foeth, H.; Fokitis, E.; Fulda-Quenzer, F.; Fuster, J.; Gandelman, M.; Garcia, C.; Gavillet, Ph.; Gazis, E.; Gokieli, R.; Golob, B.; Gomez-Ceballos, G.; Goncalves, P.; Graziani, E.; Grosdidier, G.; Grzelak, K.; Guy, J.; Haag, C.; Hallgren, A.; Hamacher, K.; Hamilton, K.; Haug, S.; Hauler, F.; Hedberg, V.; Hennecke, M.; Herr, H.; Hoffman, J.; Holmgren, S.-O.; Holt, P. J.; Houlden, M. A.; Jackson, J. N.; Jarlskog, G.; Jarry, P.; Jeans, D.; Johansson, E. K.; Jonsson, P.; Joram, C.; Jungermann, L.; Kapusta, F.; Katsanevas, S.; Katsoufis, E.; Kernel, G.; Kersevan, B. P.; Kerzel, U.; King, B. T.; Kjaer, N. J.; Kluit, P.; Kokkinias, P.; Kourkoumelis, C.; Kouznetsov, O.; Krumstein, Z.; Kucharczyk, M.; Lamsa, J.; Leder, G.; Ledroit, F.; Leinonen, L.; Leitner, R.; Lemonne, J.; Lepeltier, V.; Lesiak, T.; Liebig, W.; Liko, D.; Lipniacka, A.; Lopes, J. H.; Lopez, J. M.; Loukas, D.; Lutz, P.; Lyons, L.; MacNaughton, J.; Malek, A.; Maltezos, S.; Mandl, F.; Marco, J.; Marco, R.; Marechal, B.; Margoni, M.; Marin, J.-C.; Mariotti, C.; Markou, A.; Martinez-Rivero, C.; Masik, J.; Mastroyiannopoulos, N.; Matorras, F.; Matteuzzi, C.; Mazzucato, F.; Mazzucato, M.; Nulty, R. Mc; Meroni, C.; Migliore, E.; Mitaroff, W.; Mjoernmark, U.; Moa, T.; Moch, M.; Moenig, K.; Monge, R.; Montenegro, J.; Moraes, D.; Moreno, S.; Morettini, P.; Mueller, U.; Muenich, K.; Mulders, M.; Mundim, L.; Murray, W.; Muryn, B.; Myatt, G.; Myklebust, T.; Nassiakou, M.; Navarria, F.; Nawrocki, K.; Nicolaidou, R.; Nikolenko, M.; Oblakowska-Mucha, A.; Obraztsov, V.; Olshevski, A.; Onofre, A.; Orava, R.; Osterberg, K.; Ouraou, A.; Oyanguren, A.; Paganoni, M.; Paiano, S.; Palacios, J. P.; Palka, H.; Papadopoulou, Th. D.; Pape, L.; Parkes, C.; Parodi, F.; Parzefall, U.; Passeri, A.; Passon, O.; Peralta, L.; Perepelitsa, V.; Perrotta, A.; Petrolini, A.; Piedra, J.; Pieri, L.; Pierre, F.; Pimenta, M.; Piotto, E.; Podobnik, T.; Poireau, V.; Pol, M. E.; Polok, G.; Pozdniakov, V.; Pukhaeva, N.; Pullia, A.; Rames, J.; Read, A.; Rebecchi, P.; Rehn, J.; Reid, D.; Reinhardt, R.; Renton, P.; Richard, F.; Ridky, J.; Rivero, M.; Rodriguez, D.; Romero, A.; Ronchese, P.; Roudeau, P.; Rovelli, T.; Ruhlmann-Kleider, V.; Ryabtchikov, D.; Sadovsky, A.; Salmi, L.; Salt, J.; Sander, C.; Savoy-Navarro, A.; Schwickerath, U.; Sekulin, R.; Siebel, M.; Sisakian, A.; Smadja, G.; Smirnova, O.; Sokolov, A.; Sopczak, A.; Sosnowski, R.; Spassov, T.; Stanitzki, M.; Stocchi, A.; Strauss, J.; Stugu, B.; Szczekowski, M.; Szeptycka, M.; Szumlak, T.; Tabarelli, T.; Tegenfeldt, F.; Timmermans, J.; Tkatchev, L.; Tobin, M.; Todorovova, S.; Tome, B.; Tonazzo, A.; Tortosa, P.; Travnicek, P.; Treille, D.; Tristram, G.; Trochimczuk, M.; Troncon, C.; Turluer, M.-L.; Tyapkin, I. A.; Tyapkin, P.; Tzamarias, S.; Uvarov, V.; Valenti, G.; van Dam, P.; van Eldik, J.; van Remortel, N.; van Vulpen, I.; Vegni, G.; Veloso, F.; Venus, W.; Verdier, P.; Verzi, V.; Vilanova, D.; Vitale, L.; Vrba, V.; Wahlen, H.; Washbrook, A. J.; Weiser, C.; Wicke, D.; Wickens, J.; Wilkinson, G.; Winter, M.; Witek, M.; Yushchenko, O.; Zalewska, A.; Zalewski, P.; Zavrtanik, D.; Zhuravlov, V.; Zimin, N. I.; Zintchenko, A.; Zupan, M.

    2008-01-01

    A first measurement of the average polarisation P of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value P=-0.164±0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.

  19. Measurement of the tau lepton polarisation at LEP2

    NASA Astrophysics Data System (ADS)

    Abdallah, J.; Abreu, P.; Adam, W.; Adzic, P.; Albrecht, T.; Alemany-Fernandez, R.; Allmendinger, T.; Allport, P. P.; Amaldi, U.; Amapane, N.; Amato, S.; Anashkin, E.; Andreazza, A.; Andringa, S.; Anjos, N.; Antilogus, P.; Apel, W.-D.; Arnoud, Y.; Ask, S.; Asman, B.; Augustin, J. E.; Augustinus, A.; Baillon, P.; Ballestrero, A.; Bambade, P.; Barbier, R.; Bardin, D.; Barker, G. J.; Baroncelli, A.; Battaglia, M.; Baubillier, M.; Becks, K.-H.; Begalli, M.; Behrmann, A.; Ben-Haim, E.; Benekos, N.; Benvenuti, A.; Berat, C.; Berggren, M.; Bertrand, D.; Besancon, M.; Besson, N.; Bloch, D.; Blom, M.; Bluj, M.; Bonesini, M.; Boonekamp, M.; Booth, P. S. L.; Borisov, G.; Botner, O.; Bouquet, B.; Bowcock, T. J. V.; Boyko, I.; Bracko, M.; Brenner, R.; Brodet, E.; Bruckman, P.; Brunet, J. M.; Buschbeck, B.; Buschmann, P.; Calvi, M.; Camporesi, T.; Canale, V.; Carena, F.; Castro, N.; Cavallo, F.; Chapkin, M.; Charpentier, Ph.; Checchia, P.; Chierici, R.; Chliapnikov, P.; Chudoba, J.; Chung, S. U.; Cieslik, K.; Collins, P.; Contri, R.; Cosme, G.; Cossutti, F.; Costa, M. J.; Crennell, D.; Cuevas, J.; D'Hondt, J.; da Silva, T.; da Silva, W.; Dedovich, D.; Ricca, G. Della; de Angelis, A.; de Boer, W.; de Clercq, C.; de Lotto, B.; de Maria, N.; de Min, A.; de Paula, L.; di Ciaccio, L.; di Simone, A.; Doroba, K.; Drees, J.; Eigen, G.; Ekelof, T.; Ellert, M.; Elsing, M.; Santo, M. C. Espirito; Fanourakis, G.; Fassouliotis, D.; Feindt, M.; Fernandez, J.; Ferrer, A.; Ferro, F.; Flagmeyer, U.; Foeth, H.; Fokitis, E.; Fulda-Quenzer, F.; Fuster, J.; Gandelman, M.; Garcia, C.; Gavillet, Ph.; Gazis, E.; Gokieli, R.; Golob, B.; Gomez-Ceballos, G.; Goncalves, P.; Graziani, E.; Grosdidier, G.; Grzelak, K.; Guy, J.; Haag, C.; Hallgren, A.; Hamacher, K.; Hamilton, K.; Haug, S.; Hauler, F.; Hedberg, V.; Hennecke, M.; Herr, H.; Hoffman, J.; Holmgren, S.-O.; Holt, P. J.; Houlden, M. A.; Jackson, J. N.; Jarlskog, G.; Jarry, P.; Jeans, D.; Johansson, E. K.; Jonsson, P.; Joram, C.; Jungermann, L.; Kapusta, F.; Katsanevas, S.; Katsoufis, E.; Kernel, G.; Kersevan, B. P.; Kerzel, U.; King, B. T.; Kjaer, N. J.; Kluit, P.; Kokkinias, P.; Kourkoumelis, C.; Kouznetsov, O.; Krumstein, Z.; Kucharczyk, M.; Lamsa, J.; Leder, G.; Ledroit, F.; Leinonen, L.; Leitner, R.; Lemonne, J.; Lepeltier, V.; Lesiak, T.; Liebig, W.; Liko, D.; Lipniacka, A.; Lopes, J. H.; Lopez, J. M.; Loukas, D.; Lutz, P.; Lyons, L.; MacNaughton, J.; Malek, A.; Maltezos, S.; Mandl, F.; Marco, J.; Marco, R.; Marechal, B.; Margoni, M.; Marin, J.-C.; Mariotti, C.; Markou, A.; Martinez-Rivero, C.; Masik, J.; Mastroyiannopoulos, N.; Matorras, F.; Matteuzzi, C.; Mazzucato, F.; Mazzucato, M.; Nulty, R. Mc; Meroni, C.; Migliore, E.; Mitaroff, W.; Mjoernmark, U.; Moa, T.; Moch, M.; Moenig, K.; Monge, R.; Montenegro, J.; Moraes, D.; Moreno, S.; Morettini, P.; Mueller, U.; Muenich, K.; Mulders, M.; Mundim, L.; Murray, W.; Muryn, B.; Myatt, G.; Myklebust, T.; Nassiakou, M.; Navarria, F.; Nawrocki, K.; Nicolaidou, R.; Nikolenko, M.; Oblakowska-Mucha, A.; Obraztsov, V.; Olshevski, A.; Onofre, A.; Orava, R.; Osterberg, K.; Ouraou, A.; Oyanguren, A.; Paganoni, M.; Paiano, S.; Palacios, J. P.; Palka, H.; Papadopoulou, Th. D.; Pape, L.; Parkes, C.; Parodi, F.; Parzefall, U.; Passeri, A.; Passon, O.; Peralta, L.; Perepelitsa, V.; Perrotta, A.; Petrolini, A.; Piedra, J.; Pieri, L.; Pierre, F.; Pimenta, M.; Piotto, E.; Podobnik, T.; Poireau, V.; Pol, M. E.; Polok, G.; Pozdniakov, V.; Pukhaeva, N.; Pullia, A.; Rames, J.; Read, A.; Rebecchi, P.; Rehn, J.; Reid, D.; Reinhardt, R.; Renton, P.; Richard, F.; Ridky, J.; Rivero, M.; Rodriguez, D.; Romero, A.; Ronchese, P.; Roudeau, P.; Rovelli, T.; Ruhlmann-Kleider, V.; Ryabtchikov, D.; Sadovsky, A.; Salmi, L.; Salt, J.; Sander, C.; Savoy-Navarro, A.; Schwickerath, U.; Sekulin, R.; Siebel, M.; Sisakian, A.; Smadja, G.; Smirnova, O.; Sokolov, A.; Sopczak, A.; Sosnowski, R.; Spassov, T.; Stanitzki, M.; Stocchi, A.; Strauss, J.; Stugu, B.; Szczekowski, M.; Szeptycka, M.; Szumlak, T.; Tabarelli, T.; Tegenfeldt, F.; Timmermans, J.; Tkatchev, L.; Tobin, M.; Todorovova, S.; Tome, B.; Tonazzo, A.; Tortosa, P.; Travnicek, P.; Treille, D.; Tristram, G.; Trochimczuk, M.; Troncon, C.; Turluer, M.-L.; Tyapkin, I. A.; Tyapkin, P.; Tzamarias, S.; Uvarov, V.; Valenti, G.; van Dam, P.; van Eldik, J.; van Remortel, N.; van Vulpen, I.; Vegni, G.; Veloso, F.; Venus, W.; Verdier, P.; Verzi, V.; Vilanova, D.; Vitale, L.; Vrba, V.; Wahlen, H.; Washbrook, A. J.; Weiser, C.; Wicke, D.; Wickens, J.; Wilkinson, G.; Winter, M.; Witek, M.; Yushchenko, O.; Zalewska, A.; Zalewski, P.; Zavrtanik, D.; Zhuravlov, V.; Zimin, N. I.; Zintchenko, A.; Zupan, M.; Delphi Collaboration

    2008-01-01

    A first measurement of the average polarisation Pτ of tau leptons produced in e+e- annihilation at energies significantly above the Z resonance is presented. The polarisation is determined from the kinematic spectra of tau hadronic decays. The measured value Pτ = - 0.164 ± 0.125 is consistent with the Standard Model prediction for the mean LEP energy of 197 GeV.

  20. Tau imaging: early progress and future directions.

    PubMed

    Villemagne, Victor L; Fodero-Tavoletti, Michelle T; Masters, Colin L; Rowe, Christopher C

    2015-01-01

    Use of selective in-vivo tau imaging will enable improved understanding of tau aggregation in the brain, facilitating research into causes, diagnosis, and treatment of major tauopathies such as Alzheimer's disease, progressive supranuclear palsy, corticobasal syndrome, chronic traumatic encephalopathy, and some variants of frontotemporal lobar degeneration. Neuropathological studies of Alzheimer's disease show a strong association between tau deposits, decreased cognitive function, and neurodegenerative changes. Selective tau imaging will allow the in-vivo exploration of such associations and measure the global and regional changes in tau deposits over time. Such imaging studies will comprise non-invasive assessment of the spatial and temporal pattern of tau deposition over time, providing insight into the role tau plays in ageing and helping to establish the relation between cognition, genotype, neurodegeneration, and other biomarkers. Once validated, selective tau imaging might be useful as a diagnostic, prognostic, and progression biomarker, and a surrogate marker for the monitoring of efficacy and patient recruitment for anti-tau therapeutic trials. PMID:25496902

  1. Formation and Propagation of Tau Oligomeric Seeds

    PubMed Central

    Gerson, Julia E.; Kayed, Rakez

    2013-01-01

    Tau misfolding and aggregation leads to the formation of neurofibrillary tangles (NFTs), which have long been considered one of the main pathological hallmarks for numerous neurodegenerative diseases known as tauopathies, including Alzheimer’s Disease (AD) and Parkinson’s Disease (PD). However, recent studies completed both in vitro and in vivo suggest that intermediate forms of tau, known as tau oligomers, between the monomeric form and NFTs are the true toxic species in disease and the best targets for anti-tau therapies. However, the exact mechanism by which the spread of pathology occurs is unknown. Evidence suggests that tau oligomers may act as templates for the misfolding of native tau, thereby seeding the spread of the toxic forms of the protein. Recently, researchers have reported the ability of tau oligomers to enter and exit cells, propagating from disease-affected regions to unaffected areas. While the mechanism by which the spreading of misfolded tau occurs has yet to be elucidated, there are a few different models which have been proposed, including cell membrane stress and pore-formation, endocytosis and exocytosis, and non-traditional secretion of protein not enclosed by a membrane. Coming to an understanding of how toxic tau species seed and spread through the brain will be crucial to finding effective treatments for neurodegenerative tauopathies. PMID:23882255

  2. In vivo tau imaging: obstacles and progress.

    PubMed

    Villemagne, Victor L; Okamura, Nobuyuki

    2014-06-01

    The military conflicts of the last decade have highlighted the growing problem of traumatic brain injury in combatants returning from the battlefield. The considerable evidence pointing at the accumulation of tau aggregates and its recognition as a risk factor in neurodegenerative conditions such as Alzheimer's disease have led to a major effort to develop selective tau ligands that would allow research into the physiopathologic underpinnings of traumatic brain injury and chronic traumatic encephalopathy in military personnel and the civilian population. These tracers will allow new insights into tau pathology in the human brain, facilitating research into causes, diagnosis, and treatment of traumatic encephalopathy and major neurodegenerative dementias, such as Alzheimer's disease and some variants of frontotemporal lobar degeneration, in which tau plays a role. The field of selective tau imaging has to overcome several obstacles, some of them associated with the idiosyncrasies of tau aggregation and others related to radiotracer design. A worldwide effort has focused on the development of imaging agents that will allow selective tau imaging in vivo. Recent progress in the development of these tracers is enabling the noninvasive assessment of the extent of tau pathology in the brain, eventually allowing the quantification of changes in tau pathology over time and its relation to cognitive performance, brain volumetrics, and other biomarkers, as well as assessment of efficacy and patient recruitment for antitau therapeutic trials. PMID:24924676

  3. Tau regulates the subcellular localization of calmodulin

    SciTech Connect

    Barreda, Elena Gomez de

    2011-05-13

    Highlights: {yields} In this work we have tried to explain how a cytoplasmic protein could regulate a cell nuclear function. We have tested the role of a cytoplasmic protein (tau) in regulating the expression of calbindin gene. We found that calmodulin, a tau-binding protein with nuclear and cytoplasmic localization, increases its nuclear localization in the absence of tau. Since nuclear calmodulin regulates calbindin expression, a decrease in nuclear calmodulin, due to the presence of tau that retains it at the cytoplasm, results in a change in calbindin expression. -- Abstract: Lack of tau expression in neuronal cells results in a change in the expression of few genes. However, little is known about how tau regulates gene expression. Here we show that the presence of tau could alter the subcellular localization of calmodulin, a protein that could be located at the cytoplasm or in the nucleus. Nuclear calmodulin binds to co-transcription factors, regulating the expression of genes like calbindin. In this work, we have found that in neurons containing tau, a higher proportion of calmodulin is present in the cytoplasm compared with neurons lacking tau and that an increase in cytoplasmic calmodulin correlates with a higher expression of calbindin.

  4. TAUOLA for simulation of tau decay and production: perspectives for precision low energy and LHC applications

    NASA Astrophysics Data System (ADS)

    Wąs, Z.

    2011-09-01

    The status of Monte Carlo system for the simulation of τ-lepton production and decay in high-energy accelerator experiments is reviewed. Since the previous τ-lepton conference in 2008 some practical modifications have been introduced: (i) For the TAUOLA Monte Carlo generator of τ-lepton decays, automated and simultaneous use of many versions of form-factors for the calculation of optional weights for fits was developed and checked to work in the Belle and BaBar software environment. Work on alternative parametrizations of hadronic decays is advanced. (ii) the TAUOLA universal interface based on HepMC (the C++ event record) is now public. A similar interface for PHOTOS is now also public. (iii) Extension of the PHOTOS Monte Carlo for QED bremsstrahlung in decays featuring kernels based on complete first order matrix element are gradually becoming widely available thanks to properties of the new, HepMC based interface. (iv) Systematic tests of the programs with the help of MC-TESTER are now available for FORTRAN and C++ users. The results presented here illustrate the status of the projects performed in collaboration with Nadia Davidson, Piotr Golonka, Gizo Nanava, Tomasz Przedziński, Olga Shekhovtsova, Elżbieta Richter-W̨as, Pablo Roig, Qingjun Xu and others.

  5. Caspase-cleaved tau exhibits rapid memory impairment associated with tau oligomers in a transgenic mouse model.

    PubMed

    Kim, YoungDoo; Choi, Hyunwoo; Lee, WonJae; Park, Hyejin; Kam, Tae-In; Hong, Se-Hoon; Nah, Jihoon; Jung, Sunmin; Shin, Bora; Lee, Huikyong; Choi, Tae-Yong; Choo, Hyosun; Kim, Kyung-Keun; Choi, Se-Young; Kayed, Rakez; Jung, Yong-Keun

    2016-03-01

    In neurodegenerative diseases like AD, tau forms neurofibrillary tangles, composed of tau protein. In the AD brain, activated caspases cleave tau at the 421th Asp, generating a caspase-cleaved form of tau, TauC3. Although TauC3 is known to assemble rapidly into filaments in vitro, a role of TauC3 in vivo remains unclear. Here, we generated a transgenic mouse expressing human TauC3 using a neuron-specific promoter. In this mouse, we found that human TauC3 was expressed in the hippocampus and cortex. Interestingly, TauC3 mice showed drastic learning and spatial memory deficits and reduced synaptic density at a young age (2-3months). Notably, tau oligomers as well as tau aggregates were found in TauC3 mice showing memory deficits. Further, i.p. or i.c.v. injection with methylene blue or Congo red, inhibitors of tau aggregation in vitro, and i.p. injection with rapamycin significantly reduced the amounts of tau oligomers in the hippocampus, rescued spine density, and attenuated memory impairment in TauC3 mice. Together, these results suggest that TauC3 facilitates early memory impairment in transgenic mice accompanied with tau oligomer formation, providing insight into the role of TauC3 in the AD pathogenesis associated with tau oligomers and a useful AD model to test drug candidates. PMID:26704708

  6. Detecting tau in serum of transgenic animal models after tau immunotherapy treatment.

    PubMed

    d'Abramo, Cristina; Acker, Christopher M; Schachter, Joel B; Terracina, Giuseppe; Wang, Xiaohai; Forest, Stefanie K; Davies, Peter

    2016-01-01

    In the attempt to elucidate if the "peripheral sink hypothesis" could be a potential mechanism of action for tau removal in passive immunotherapy experiments, we have examined tau levels in serum of chronically injected JNPL3 and Tg4510 transgenic animals. Measurement of tau in serum of mice treated with tau antibodies is challenging because of the antibody interference in sandwich enzyme-linked immunosorbent assays. To address this issue, we have developed a heat-treatment protocol at acidic pH to remove interfering molecules from serum, with excellent recovery of tau. The present data show that pan-tau and conformational antibodies do increase tau in mouse sera. However, these concentrations in serum do not consistently correlate with reductions of tau pathology in brain, suggesting that large elevations of tau species measured in serum are not predictive of efficacy. Here, we describe a reliable method to detect tau in serum of transgenic animals that have undergone tau immunotherapy. Levels of tau in human serum are less than the sensitivity of current assays, although artifactual signals are common. The method may be useful in similarly treated humans, a situation in which false positive signals are likely. PMID:26508157

  7. The Microjet of AA Tau

    NASA Astrophysics Data System (ADS)

    Cox, A. W.; Hilton, G. M.; Williger, G. M.; Grady, C. A.; Woodgate, B.

    2005-12-01

    The microjet of AA Tau A.W. Cox (Atholton High School, Columbia MD), G.M. Hilton (SSAI and GSFC), G.M. Williger (JHU and U. Louisville), C.A. Grady (Eureka Scientific and GSFC) B.Woodgate (NASA's GSFC) AA Tau is a classical T Tauri star with a spatially resolved disk viewed at approximately 70 degrees from pole-on. Photo-polarimetric variability of the star has been interpreted as being caused by the stellar magnetic field being inclined at 30 degrees with respect to the stellar rotation axis, producing a warp in the inner disk. Under these conditions, any jet should be less collimated than typical of T Tauri microjets, and should show signs of the jet axis precessing around the stellar rotation axis. When compared with the microjets imaged in the HST/STIS coronagraphic imaging survey, the AA Tau jet has an opening half-angle of approximately 10-15 degrees rather than the 3-5 degrees typical of the other T Tauri stars which have been coronagraphically imaged by HST/STIS. Using the HST data with ultra-narrowband imagery and long slit spectroscopy obtained with the Goddard Fabry-Perot and the Dual Imaging Spectrograph at the Apache Point Observatory 3.5m telescope, we derive the jet inclination, knot ejection epochs, and ejection frequency. We also compare the jet opening angle with model predictions. Apache Point Observatory observations with the Goddard Fabry-Perot were made through a grant of Director's Discretionary Time. Apache Point Observatory is operated by the Astrophysical Research Consortium. The GFP was supported under NASA RTOP 51-188-01-22 to GSFC. Grady is supported under NASA contract NNH05CD30C to Eureka Scientific.

  8. Analysis of BaBar data for three meson tau decay modes using the Tauola generator

    DOE PAGESBeta

    Shekhovtsova, Olga

    2014-11-24

    The hadronic current for the τ⁻ → π⁻π⁺π⁻ντ decay calculated in the framework of the Resonance Chiral Theory with an additional modification to include the σ meson is described. In addition, implementation into the Monte Carlo generator Tauola and fitting strategy to get the model parameters using the one-dimensional distributions are discussed. The results of the fit to one-dimensional mass invariant spectrum of the BaBar data are presented.

  9. Analysis of BaBar data for three meson tau decay modes using the Tauola generator

    SciTech Connect

    Shekhovtsova, Olga

    2014-11-24

    The hadronic current for the τ⁻ → π⁻π⁺π⁻ντ decay calculated in the framework of the Resonance Chiral Theory with an additional modification to include the σ meson is described. In addition, implementation into the Monte Carlo generator Tauola and fitting strategy to get the model parameters using the one-dimensional distributions are discussed. The results of the fit to one-dimensional mass invariant spectrum of the BaBar data are presented.

  10. The microtubule-associated tau protein has intrinsic acetyltransferase activity.

    PubMed

    Cohen, Todd J; Friedmann, Dave; Hwang, Andrew W; Marmorstein, Ronen; Lee, Virginia M Y

    2013-06-01

    Tau proteins are the building blocks of neurofibrillary tangles (NFTs) found in a range of neurodegenerative tauopathies, including Alzheimer's disease. Recently, we demonstrated that tau is extensively post-translationally modified by lysine acetylation, which impairs normal tau function and promotes pathological aggregation. Identifying the enzymes that mediate tau acetylation could provide targets for future therapies aimed at reducing the burden of acetylated tau. Here, we report that mammalian tau proteins possess intrinsic enzymatic activity capable of catalyzing self-acetylation. Functional mapping of tau acetyltransferase activity followed by biochemical analysis revealed that tau uses catalytic cysteine residues in the microtubule-binding domain to facilitate tau lysine acetylation, thus suggesting a mechanism similar to that employed by MYST-family acetyltransferases. The identification of tau as an acetyltransferase provides a framework to further understand tau pathogenesis and highlights tau enzymatic activity as a potential therapeutic target. PMID:23624859

  11. Csf p-tau181/tau ratio as biomarker for TDP pathology in frontotemporal dementia.

    PubMed

    Borroni, Barbara; Benussi, Alberto; Archetti, Silvana; Galimberti, Daniela; Parnetti, Lucilla; Nacmias, Benedetta; Sorbi, Sandro; Scarpini, Elio; Padovani, Alessandro

    2015-03-01

    Our objective was to evaluate the CSF phospho-Tau181/total-Tau (p/t-Tau) ratio to distinguish between the two main forms of frontotemporal lobar degeneration (FTLD): FTLD with TDP-43 (FTLD-TDP) and FTLD with Tau inclusions (FTLD-Tau). CSF p/t-Tau ratio was examined in 79 FTLD patients with predictable neuropathology, i.e. Tau (affected by progressive supranuclear palsy or carriers of mutations within the MAPT gene) or TDP-43 (carriers of mutations within granulin, C9orf72, TARDBP genes or affected by FTD with motor neuron disease). FTLD patients were randomly grouped in a training cohort (n = 39) to assess the best CSF p/t-Tau cut-off score according to ROC analysis, and a validation cohort (n = 40) to evaluate accuracy values of the identified marker. Results showed that, in the training cohort, we found a significantly reduced CSF p/t-Tau ratio in FTLD-TDP relative to FTLD-Tau. ROC analysis for p/t-Tau ratio was 0.873 and cut-off score of 0.136 allowed to differentiate FTLD-TDP and FTLD-Tau with 81.8% sensitivity and 88.2% specificity, respectively. Analysis in the validation cohort showed CSF p/t-Tau ratio < 0.136 to distinguish FTLD-TDP from FTLD-Tau with 83.3% specificity and 63.6% sensitivity, respectively. The positive predictive value of detecting TDP neuropathology was 82.4%. In conclusion, a reduced CSF p/t-Tau ratio represents a viable biomarker to correctly identify TDP pathology in FTLD. PMID:25352065

  12. Tau assembly in inducible transfectants expressing wild-type or FTDP-17 tau.

    PubMed

    DeTure, Michael; Ko, Li-Wen; Easson, Colin; Yen, Shu-Hui

    2002-11-01

    Conditional expression systems for 4-repeat wild-type (WT) tau or the corresponding mutants V337M and R406W were established in human neuroglioma H4 cells to study the effect of tau mutations on the physicochemical properties of tau, and to develop a cellular model for the formation of filamentous tau characteristic of frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17) and Alzheimer's disease. Upon induction tau expression increased, reaching maximal levels at 5 to 7 days. WT tau was phosphorylated at amino acids T181, S202/T205, T231, and S396/S404. The R406W mutation decreased tau phosphorylation at each of these sites as did the V337M mutation except for S396/S404 sites that increased. Most tau in postnuclear cell lysates was recovered in the supernatant fraction after centrifugation at 200,000 x g. The amount of tau in the pellet fraction increased more in mutant transfectants compared to WT when the induction was extended beyond 5 days. This particulate tau could be partially extracted with salt, Triton X-100, or sarkosyl. Of the transfectants, R406W had the highest proportion of sarkosyl-insoluble tau by day 7. This insoluble fraction was thioflavin S-positive and contained 15- to 5-nm-wide filaments with tau immunoreactivities. The R406W filaments were more abundant than those detected in similar preparations from WT or V337M transfectants. At the light microscopy level, most tau was found with microtubules, or diffusely distributed in the cytoplasm, but none of this appeared thioflavin S-positive. The results suggest that conditional tau transfectants are in a pretangle stage making them an attractive model system for studying intracellular tangle accumulation and for testing potential therapeutic agents as inhibitors for tau aggregation. PMID:12414518

  13. Prospect for measuring the CP phase in the $$h\\tau\\tau$$ coupling at the LHC

    DOE PAGESBeta

    Askew, Andrew; Jaiswal, Prerit; Okui, Takemichi; Prosper, Harrison B.; Sato, Nobuo

    2015-04-01

    The search for a new source of CP violation is one of the most important endeavors in particle physics. A particularly interesting way to perform this search is to probe the CP phase in themore » $$h\\tau\\tau$$ coupling, as the phase is currently completely unconstrained by all existing data. Recently, a novel variable $$\\Theta$$ was proposed for measuring the CP phase in the $$h\\tau\\tau$$ coupling through the $$\\tau^\\pm \\to \\pi^\\pm \\pi^0 \

  14. Tau pathology in two Dutch families with mutations in the microtubule-binding region of tau.

    PubMed

    Spillantini, M G; Crowther, R A; Kamphorst, W; Heutink, P; van Swieten, J C

    1998-11-01

    Different mutations in the microtubule-associated tau protein gene have recently been identified in several families with hereditary frontotemporal dementia and Parkinsonism (FTDP-17) linked to chromosome 17q21-22. Some families show neuronal and glial deposits containing hyperphosphorylated tau in several brain regions. We have investigated the presence of tau deposits by using a panel of anti-tau antibodies in three brains of a family with the P301L mutation (HFTD1) and in another family with the G272V mutation (HFTD2) of the tau gene. Numerous intracytoplasmic tau deposits in neurons, glial cells, and neurites were found in hippocampal formation, neocortex, and substantia nigra. These deposits in three patients from HFTD1 consisted of slender twisted filaments 15 nm wide with variable periodicity and a few straight filaments. Tau extracted from these filaments appeared as two major bands of 64 and 68 kd and a minor band of 72 kd that, after alkaline phosphatase treatment, proved to consist mainly of 4-repeat tau isoforms and one of the 3-repeat isoforms. In three patients from HFTD2 numerous Pick-like bodies were present. The conclusion is that the type and distribution of tau deposits in HFTD1 and HFTD2, the physical structure of filaments, and tau isoform composition in HFTD1 differ from Alzheimer's disease and an FTDP-17 family with a V337M mutation in the tau gene. PMID:9811325

  15. A novel tau transcript in cultured human neuroblastoma cells expressing nuclear tau

    PubMed Central

    1993-01-01

    We previously reported the presence of the microtubule-associated protein, tau in the nuclei of primate cells in culture. The present study confirms the existence of nuclear tau in two human neuroblastoma cells lines by indirect immunofluorescence and Western blot using mAbs to tau. Northern blot analysis of poly A+ mRNA detects a novel 2-kb tau transcript coexpressed with the 6-kb message in cultured human cells and human frontal cortex. PCR and cDNA sequencing demonstrate that the 2-kb message contains the entire tau coding region. Furthermore, actinomycin D transcription inhibition experiments indicate that the 2- kb message is not derived from the 6-kb message, but instead arises from the original tau transcript. One of the human neuroblastoma cell lines examined contains both nuclear and cytoplasmic tau as assayed by both Western blot and indirect immunofluorescence. Northern blot analysis of this cell line indicates that copious amounts of the 2-kb message are present while little of the 6-kb transcript is obvious. Immunofluorescence analysis of this cell line demonstrates that the cytoplasmic tau is not localized to microtubules. Together, these results indicate that the 2-kb tau message in humans may specify tau for non-microtubule functions in both the cytoplasm and the nucleus. We hypothesize that this is accomplished via a message targeting mechanism mediated by the untranslated regions of the tau messages. PMID:8468346

  16. Physics with tau leptons at CDF

    SciTech Connect

    Hays, C.P.; /Oxford U.

    2007-04-01

    The {radical}s = 1.96 TeV p{bar p} collisions produced by the Tevatron result in many processes with tau leptons in the final state. The CDF Collaboration has studied these final states in Z and t{bar t} production, and has used tau leptons to search for evidence of Higgs, sparticle, and Z{prime} production.

  17. Elevated cerebrospinal fluid tau in Wernicke encephalopathy.

    PubMed

    Frijlink, Daphne W; Tilanus, Joachim J; Roks, Gerwin

    2012-01-01

    Wernicke encephalopathy (WE) commonly presents with oculomotor abnormalities, gait ataxia and confusion. WE can mimic rapidly progressive dementia syndromes, such as Creutzfeldt-Jakob disease (CJD). Cerebrospinal fluid (CSF) tau is frequently used for diagnosis of several dementia subtypes, predominantly CJD and Alzheimer's disease. The combination of very high CSF tau (tau) and normal phosphorylated tau (p-tau) levels is almost exclusively seen in aggressive diseases, such as CJD. The authors present a case of a woman with WE, caused by chronic insufficient dietary intake, with highly elevated CSF tau and normal p-tau. The clinical symptoms and CSF findings raised the suspicion of CJD. However, shortly after immediate treatment with thiamine the patient clinically improved. At follow-up, 2.5 months later, she had made a good recovery. This case of rapidly progressive dementia illustrates that, even in the case of a highly elevated CSF tau, clinicians should be alert for treatable causes such as WE. PMID:22879004

  18. Tau phosphorylation affects its axonal transport and degradation

    PubMed Central

    Rodríguez-Martín, Teresa; Cuchillo-Ibáñez, Inmaculada; Noble, Wendy; Nyenya, Fanon; Anderton, Brian H.; Hanger, Diane P.

    2013-01-01

    Phosphorylated forms of microtubule-associated protein tau accumulate in neurofibrillary tangles in Alzheimer's disease. To investigate the effects of specific phosphorylated tau residues on its function, wild type or phosphomutant tau was expressed in cells. Elevated tau phosphorylation decreased its microtubule binding and bundling, and increased the number of motile tau particles, without affecting axonal transport kinetics. In contrast, reducing tau phosphorylation enhanced the amount of tau bound to microtubules and inhibited axonal transport of tau. To determine whether differential tau clearance is responsible for the increase in phosphomimic tau, we inhibited autophagy in neurons which resulted in a 3-fold accumulation of phosphomimic tau compared with wild type tau, and endogenous tau was unaffected. In autophagy-deficient mouse embryonic fibroblasts, but not in neurons, proteasomal degradation of phosphomutant tau was also reduced compared with wild type tau. Therefore, autophagic and proteasomal pathways are involved in tau degradation, with autophagy appearing to be the primary route for clearing phosphorylated tau in neurons. Defective autophagy might contribute to the accumulaton of tau in neurodegenerative diseases. PMID:23601672

  19. Microglial internalization and degradation of pathological tau is enhanced by an anti-tau monoclonal antibody

    PubMed Central

    Luo, Wenjie; Liu, Wencheng; Hu, Xiaoyan; Hanna, Mary; Caravaca, April; Paul, Steven M.

    2015-01-01

    Microglia have been shown to contribute to the clearance of brain amyloid ? peptides (A?), the major component of amyloid plaques, in Alzheimers disease (AD). However, it is not known whether microglia play a similar role in the clearance of tau, the major component of neurofibrillary tangles (NFTs). We now report that murine microglia rapidly internalize and degrade hyperphosphorylated pathological tau isolated from AD brain tissue in a time-dependent manner in vitro. We further demonstrate that microglia readily degrade human tau species released from AD brain sections and eliminate NFTs from brain sections of P301S tauopathy mice. The anti-tau monoclonal antibody MC1 enhances microglia-mediated tau degradation in an Fc-dependent manner. Our data identify a potential role for microglia in the degradation and clearance of pathological tau species in brain and provide a mechanism explaining the potential therapeutic actions of passively administered anti-tau monoclonal antibodies. PMID:26057852

  20. Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neurons

    PubMed Central

    Rodríguez-Martín, Teresa; Pooler, Amy M.; Lau, Dawn H.W.; Mórotz, Gábor M.; De Vos, Kurt J.; Gilley, Jonathan; Coleman, Michael P.; Hanger, Diane P.

    2016-01-01

    Expression of the frontotemporal dementia-related tau mutation, P301L, at physiological levels in adult mouse brain (KI-P301L mice) results in overt hypophosphorylation of tau and age-dependent alterations in axonal mitochondrial transport in peripheral nerves. To determine the effects of P301L tau expression in the central nervous system, we examined the kinetics of mitochondrial axonal transport and tau phosphorylation in primary cortical neurons from P301L knock-in (KI-P301L) mice. We observed a significant 50% reduction in the number of mitochondria in the axons of cortical neurons cultured from KI-P301L mice compared to wild-type neurons. Expression of murine P301L tau did not change the speed, direction of travel or likelihood of movement of mitochondria. Notably, the angle that defines the orientation of the mitochondria in the axon, and the volume of individual moving mitochondria, were significantly increased in neurons expressing P301L tau. We found that murine tau phosphorylation in KI-P301L mouse neurons was diminished and the ability of P301L tau to bind to microtubules was also reduced compared to tau in wild-type neurons. The P301L mutation did not influence the ability of murine tau to associate with membranes in cortical neurons or in adult mouse brain. We conclude that P301L tau is associated with mitochondrial changes and causes an early reduction in murine tau phosphorylation in neurons coupled with impaired microtubule binding of tau. These results support the association of mutant tau with detrimental effects on mitochondria and will be of significance for the pathogenesis of tauopathies. PMID:26459111

  1. Reduced number of axonal mitochondria and tau hypophosphorylation in mouse P301L tau knockin neurons.

    PubMed

    Rodrguez-Martn, Teresa; Pooler, Amy M; Lau, Dawn H W; Mrotz, Gbor M; De Vos, Kurt J; Gilley, Jonathan; Coleman, Michael P; Hanger, Diane P

    2016-01-01

    Expression of the frontotemporal dementia-related tau mutation, P301L, at physiological levels in adult mouse brain (KI-P301L mice) results in overt hypophosphorylation of tau and age-dependent alterations in axonal mitochondrial transport in peripheral nerves. To determine the effects of P301L tau expression in the central nervous system, we examined the kinetics of mitochondrial axonal transport and tau phosphorylation in primary cortical neurons from P301L knock-in (KI-P301L) mice. We observed a significant 50% reduction in the number of mitochondria in the axons of cortical neurons cultured from KI-P301L mice compared to wild-type neurons. Expression of murine P301L tau did not change the speed, direction of travel or likelihood of movement of mitochondria. Notably, the angle that defines the orientation of the mitochondria in the axon, and the volume of individual moving mitochondria, were significantly increased in neurons expressing P301L tau. We found that murine tau phosphorylation in KI-P301L mouse neurons was diminished and the ability of P301L tau to bind to microtubules was also reduced compared to tau in wild-type neurons. The P301L mutation did not influence the ability of murine tau to associate with membranes in cortical neurons or in adult mouse brain. We conclude that P301L tau is associated with mitochondrial changes and causes an early reduction in murine tau phosphorylation in neurons coupled with impaired microtubule binding of tau. These results support the association of mutant tau with detrimental effects on mitochondria and will be of significance for the pathogenesis of tauopathies. PMID:26459111

  2. Human secreted tau increases amyloid-beta production.

    PubMed

    Bright, Jessica; Hussain, Sami; Dang, Vu; Wright, Sarah; Cooper, Bonnie; Byun, Tony; Ramos, Carla; Singh, Andrew; Parry, Graham; Stagliano, Nancy; Griswold-Prenner, Irene

    2015-02-01

    The interaction of amyloid-beta (A?) and tau in the pathogenesis of Alzheimer's disease is a subject of intense inquiry, with the bulk of evidence indicating that changes in tau are downstream of A?. It has been shown however, that human tau overexpression in amyloid precursor protein transgenic mice increases A? plaque deposition. Here, we confirm that human tau increases A? levels. To determine if the observed changes in A? levels were because of intracellular or extracellular secreted tau (eTau for extracellular tau), we affinity purified secreted tau from Alzheimer's disease patient-derived cortical neuron conditioned media and analyzed it by liquid chromatography-mass spectrometry. We found the extracellular species to be composed predominantly of a series of N-terminal fragments of tau, with no evidence of C-terminal tau fragments. We characterized a subset of high affinity tau antibodies, each capable of engaging and neutralizing eTau. We found that neutralizing eTau reduces A? levels in vitro in primary human cortical neurons where exogenously adding eTau increases A? levels. In vivo, neutralizing human tau in 2 human tau transgenic models also reduced A? levels. We show that the human tau insert sequence is sufficient to cause the observed increase in A? levels. Our data furthermore suggest that neuronal hyperactivity may be the mechanism by which this regulation occurs. We show that neuronal hyperactivity regulates both eTau secretion and A? production. Electrophysiological analysis shows for the first time that secreted eTau causes neuronal hyperactivity. Its induction of hyperactivity may be the mechanism by which eTau regulates A? production. Together with previous findings, these data posit a novel connection between tau and A?, suggesting a dynamic mechanism of positive feed forward regulation. A? drives the disease pathway through tau, with eTau further increasing A? levels, perpetuating a destructive cycle. PMID:25442111

  3. The environmental toxin arsenite induces tau hyperphosphorylation.

    PubMed

    Giasson, Benoit I; Sampathu, Deepak M; Wilson, Christina A; Vogelsberg-Ragaglia, Vanessa; Mushynski, Walter E; Lee, Virginia M-Y

    2002-12-24

    Abnormally hyperphosphorylated tau polymers known as paired helical filaments constitute one of the major characteristic lesions that lead to the demise of neurons in Alzheimer's disease. Here, we demonstrate that the environmental toxin arsenite causes a significant increase in the phosphorylation of several amino acid residues (Thr-181, Ser-202, Thr-205, Thr-231, Ser-262, Ser-356, Ser-396, and Ser-404) in tau, which are also hyperphosphorylated under pathological conditions. Complementary phosphopeptide mapping revealed a dramatic increase in the (32)P-labeling of many peptides in tau following arsenite treatment. Although arsenite activates extracellular-signal regulated kinases-1/-2 and stress-activated protein kinases, these enzymes did not contribute to the arsenite-increased phosphorylation, nor did they appear to normally modify tau in vivo. Tau phosphorylation induced by arsenite did not involve glycogen synthase kinase-3 or protein phosphatase-1 or -2, but the activity responsible for tau hyperphosphorylation could be inhibited with the protein kinase inhibitor roscovitine. The effects of arsenite on the phosphorylation of some tau mutations (DeltaKappa280, V337M, and R406W) associated with frontal-temporal dementia with parkinsonism linked to chromosome 17 was analyzed. The unchallenged and arsenite-induced phosphorylation of some mutant proteins, especially R406W, was altered at several phosphorylation sites, indicating that these mutations can significantly affect the structure of tau in vivo. Although the major kinase(s) involved in aberrant tau phosphorylation remains elusive, these results indicate that environmental factors, such as arsenite, may be involved in the cascade leading to deregulation of tau function associated with neurodegeneration. PMID:12484777

  4. Endogenous tau aggregates in oligodendrocytes of rTg4510 mice induced by human P301L tau.

    PubMed

    Ren, Yan; Lin, Wen-Lang; Sanchez, Laura; Ceballos, Carolina; Polydoro, Manuela; Spires-Jones, Tara L; Hyman, Bradley T; Dickson, Dennis W; Sahara, Naruhiko

    2014-01-01

    Tau belongs to the microtubule-associated family of proteins that maintain cytoskeletal structure by regulating microtubule dynamics. In certain neurodegenerative diseases termed tauopathies, tau is abnormally phosphorylated and accumulates as filamentous inclusions. Transgenic mouse models that overexpress human tau have been widely used to investigate tau pathogenesis. Although many studies have attempted to elucidate the pathological function of transgenic human tau, it remains unknown whether endogenous mouse tau is involved in disease progression. Here we generated an mTau antibody that selectively recognizes mouse and rat tau, but not human tau. In rTg4510 tau transgenic mice, we identified a higher molecular weight mouse tau (~60-kDa) in sarkosyl-insoluble fractions. mTau antibody started to recognize intracellular aggregates and thread-like structures in 4- to 6-month-old rTg4510 mice. Tau inclusions appeared earlier, being detected in 2.5-month-old rTg4510 mice with MC1 antibody. Immunoelectron microscopy confirmed the presence of filamentous aggregates of mouse tau, which were abundant in oligodendrocytes but rare in neurons. Mouse tau inclusions in oligodendrocytes were confirmed by double-labeling with an oligodendrocyte marker. Our data indicate that mouse tau has potential aggregation properties in neurons and non-neurons. The mTau antibody will be useful for investigating the role of mouse tau in mouse models of tauopathy. PMID:24028867

  5. Characteristics of Tau and Its Ligands in PET Imaging.

    PubMed

    Harada, Ryuichi; Okamura, Nobuyuki; Furumoto, Shozo; Tago, Tetsuro; Yanai, Kazuhiko; Arai, Hiroyuki; Kudo, Yukitsuka

    2016-01-01

    Tau deposition is one of the neuropathological hallmarks in Alzheimer's disease as well as in other neurodegenerative disorders called tauopathies. Recent efforts to develop selective tau radiopharmaceuticals have allowed the visualization of tau deposits in vivo. In vivo tau imaging allows the assessment of the regional distribution of tau deposits in a single human subject over time for determining the pathophysiology of tau accumulation in aging and neurodegenerative conditions as well as for application in drug discovery of anti-dementia drugs as surrogate markers. However, tau deposits show complicated characteristics because of different isoform composition, histopathology, and ultrastructure in various neurodegenerative conditions. In addition, since tau radiopharmaceuticals possess different chemotype classes, they may show different binding characteristics with heterogeneous tau deposits. In this review, we describe the characteristics of tau deposits and their ligands that have ?-sheet binding properties, and the status of tau imaging in clinical studies. PMID:26751494

  6. Tau Reconstruction and Identification at the Compact Muon Solenoid

    NASA Astrophysics Data System (ADS)

    Friis, E. K.; CMS Collaboration

    2011-09-01

    New Physics beyond the Standard Model could appear at the LHC in final states with tau leptons. The development of efficient and accurate reconstruction and identification algorithms for taus decaying to hadrons is therefore an important item in the physics program of the Compact Muon Solenoid (CMS) experiment. New identification algorithms utilizing information about the known properties of tau hadronic decays have been recently developed and provide considerable performance improvements with respect to algorithms previously used by the CMS collaboration. Details of the strategies for identification of individual tau decay modes are presented in the following, as well as first measurements of the quark and gluon jet mis-tag rate with the first 8.4 nb of data collected at ?{s}=7 TeV.

  7. Intracellular and extracellular roles for tau in neurodegenerative disease.

    PubMed

    Hanger, Diane P; Lau, Dawn H W; Phillips, Emma C; Bondulich, Marie K; Guo, Tong; Woodward, Benjamin W; Pooler, Amy M; Noble, Wendy

    2014-01-01

    Tau has a well-established role as a microtubule-associated protein, in which it stabilizes the neuronal cytoskeleton. This function of tau is influenced by tau phosphorylation state, which is significantly increased in Alzheimer's disease and related tauopathies. Disruptions to the cytoskeleton in disease-affected neurons include reduced length and numbers of stable microtubules, and their diminished stability is associated with increased tau phosphorylation in disease. Tau is also localized in the nucleus and plasma membrane of neurons, where it could have roles in DNA repair and cell signaling. Most recently, potential roles for extracellular tau have been highlighted. The release of tau from neurons is a physiological process that can be regulated by neuronal activity and extracellular tau may play a role in inter-neuronal signaling. In addition, recent studies have suggested that the misfolding of tau in diseased brain leads to abnormal conformations of tau that can be taken up by neighboring neurons. Such a mechanism may be responsible for the apparent prion-like spreading of tau pathology through the brain, which occurs in parallel with clinical progression in the tauopathies. The relationship between tau localization in neurons, tau release, and tau uptake remains to be established, as does the function of extracellular tau. More research is needed to identify disease mechanisms that drive the release and propagation of pathogenic tau and to determine the impact of extracellular tau on cognitive decline in neurodegenerative disease. PMID:24595196

  8. HL Tau - The Missing Dust

    NASA Astrophysics Data System (ADS)

    Rettig, T.; Brittain, S.; Simon, T.; Kulesa, C.; Haywood, J.

    2004-06-01

    High-resolution infrared spectra of HL Tau exhibit broad emission lines of 12CO gas phase molecules as well as narrow absorption lines of 12CO, 13CO, and C18O. The broad emission lines of vibrationally-excited 12CO are dominated by the hot (T ~1500 K) inner-disk (radius r < 0.2 AU). The narrow absorption lines of CO are found to originate from the circumstellar gas at a temperature of ~100 K. The cooler material indicates a large column of absorbing gas along the line of sight, which indirectly implies a large amount of dust extinction. However, the minimal opacity allowed by our emission line results severely constrains the M-band extinction and suggests that there is much less dust along the line of sight than inferred from the CO absorption data.

  9. An unbiased approach to identifying tau kinases that phosphorylate tau at sites associated with Alzheimer disease.

    PubMed

    Cavallini, Annalisa; Brewerton, Suzanne; Bell, Amanda; Sargent, Samantha; Glover, Sarah; Hardy, Clare; Moore, Roger; Calley, John; Ramachandran, Devaki; Poidinger, Michael; Karran, Eric; Davies, Peter; Hutton, Michael; Szekeres, Philip; Bose, Suchira

    2013-08-01

    Neurofibrillary tangles, one of the hallmarks of Alzheimer disease (AD), are composed of paired helical filaments of abnormally hyperphosphorylated tau. The accumulation of these proteinaceous aggregates in AD correlates with synaptic loss and severity of dementia. Identifying the kinases involved in the pathological phosphorylation of tau may identify novel targets for AD. We used an unbiased approach to study the effect of 352 human kinases on their ability to phosphorylate tau at epitopes associated with AD. The kinases were overexpressed together with the longest form of human tau in human neuroblastoma cells. Levels of total and phosphorylated tau (epitopes Ser(P)-202, Thr(P)-231, Ser(P)-235, and Ser(P)-396/404) were measured in cell lysates using AlphaScreen assays. GSK3?, GSK3?, and MAPK13 were found to be the most active tau kinases, phosphorylating tau at all four epitopes. We further dissected the effects of GSK3? and GSK3? using pharmacological and genetic tools in hTau primary cortical neurons. Pathway analysis of the kinases identified in the screen suggested mechanisms for regulation of total tau levels and tau phosphorylation; for example, kinases that affect total tau levels do so by inhibition or activation of translation. A network fishing approach with the kinase hits identified other key molecules putatively involved in tau phosphorylation pathways, including the G-protein signaling through the Ras family of GTPases (MAPK family) pathway. The findings identify novel tau kinases and novel pathways that may be relevant for AD and other tauopathies. PMID:23798682

  10. Optimization and Performance of the ATLAS Tau Trigger with Cosmics Data

    NASA Astrophysics Data System (ADS)

    Shamim, Mansoora

    2010-04-01

    Tau lepton, being the heaviest of all known leptons (mT = 1776.84 0.17MeV), is of special importance. Due to its short lifetime, with (cT = 87.11?m), it decays inside the beam pipe. The identification of tau is, therefore, done through its decay products inside the detector. A tau jet can be identified through the presence of a well collimated calorimeter cluster with a small number of associated tracks. The tau lepton decays into electron or muons 35% of the time, while 65% of its decays include hadrons, mostly pions. The events where tau decays into leptons can be triggered by low ET threshold electron or muon trigger. A dedicated tau trigger has been designed and implemented at the ATLAS experiment to select events where a tau lepton decays into hadrons. Triggering on tau events will not only help in understanding the standard model (SM) processes during early running but will also increase the discovery potential of the ATLAS detector through searches for Higgs boson and supersymmetric particles at high luminosities. The cosmics-ray data at ATLAS have provided a valuable handle to optimize and commission the ATLAS detector before beam collisions. In this process the ATLAS tau trigger algorithms have been exercised and the hardware-based first level rates studied.

  11. Proteopathic tau seeding predicts tauopathy in vivo.

    PubMed

    Holmes, Brandon B; Furman, Jennifer L; Mahan, Thomas E; Yamasaki, Tritia R; Mirbaha, Hilda; Eades, William C; Belaygorod, Larisa; Cairns, Nigel J; Holtzman, David M; Diamond, Marc I

    2014-10-14

    Transcellular propagation of protein aggregates, or proteopathic seeds, may drive the progression of neurodegenerative diseases in a prion-like manner. In tauopathies such as Alzheimer's disease, this model predicts that tau seeds propagate pathology through the brain via cell-cell transfer in neural networks. The critical role of tau seeding activity is untested, however. It is unknown whether seeding anticipates and correlates with subsequent development of pathology as predicted for a causal agent. One major limitation has been the lack of a robust assay to measure proteopathic seeding activity in biological specimens. We engineered an ultrasensitive, specific, and facile FRET-based flow cytometry biosensor assay based on expression of tau or synuclein fusions to CFP and YFP, and confirmed its sensitivity and specificity to tau (∼ 300 fM) and synuclein (∼ 300 pM) fibrils. This assay readily discriminates Alzheimer's disease vs. Huntington's disease and aged control brains. We then carried out a detailed time-course study in P301S tauopathy mice, comparing seeding activity versus histological markers of tau pathology, including MC1, AT8, PG5, and Thioflavin S. We detected robust seeding activity at 1.5 mo, >1 mo before the earliest histopathological stain. Proteopathic tau seeding is thus an early and robust marker of tauopathy, suggesting a proximal role for tau seeds in neurodegeneration. PMID:25261551

  12. Simulated Cytoskeletal Collapse via Tau Degradation

    PubMed Central

    Sendek, Austin; Fuller, Henry R.; Hayre, N. Robert; Singh, Rajiv R. P.; Cox, Daniel L.

    2014-01-01

    We present a coarse-grained two dimensional mechanical model for the microtubule-tau bundles in neuronal axons in which we remove taus, as can happen in various neurodegenerative conditions such as Alzheimers disease, tauopathies, and chronic traumatic encephalopathy. Our simplified model includes (i) taus modeled as entropic springs between microtubules, (ii) removal of taus from the bundles due to phosphorylation, and (iii) a possible depletion force between microtubules due to these dissociated phosphorylated taus. We equilibrate upon tau removal using steepest descent relaxation. In the absence of the depletion force, the transverse rigidity to radial compression of the bundles falls to zero at about 60% tau occupancy, in agreement with standard percolation theory results. However, with the attractive depletion force, spring removal leads to a first order collapse of the bundles over a wide range of tau occupancies for physiologically realizable conditions. While our simplest calculations assume a constant concentration of microtubule intercalants to mediate the depletion force, including a dependence that is linear in the detached taus yields the same collapse. Applying percolation theory to removal of taus at microtubule tips, which are likely to be the protective sites against dynamic instability, we argue that the microtubule instability can only obtain at low tau occupancy, from 0.060.30 depending upon the tau coordination at the microtubule tips. Hence, the collapse we discover is likely to be more robust over a wide range of tau occupancies than the dynamic instability. We suggest in vitro tests of our predicted collapse. PMID:25162587

  13. Intracerebral injection of preformed synthetic tau fibrils initiates widespread tauopathy and neuronal loss in the brains of tau transgenic mice

    PubMed Central

    Peeraer, Eve; Bottelbergs, Astrid; Van Kolen, Kristof; Stancu, Ilie-Cosmin; Vasconcelos, Bruno; Mahieu, Michel; Duytschaever, Hilde; Ver Donck, Luc; Torremans, An; Sluydts, Ellen; Van Acker, Nathalie; Kemp, John A.; Mercken, Marc; Brunden, Kurt R.; Trojanowski, John Q.; Dewachter, Ilse; Lee, Virginia M.Y.; Moechars, Diederik

    2015-01-01

    Neurofibrillary tangles composed of hyperphosphorylated fibrillized tau are found in numerous tauopathies including Alzheimer's disease. Increasing evidence suggests that tau pathology can be transmitted from cell-to-cell; however the mechanisms involved in the initiation of tau fibrillization and spreading of disease linked to progression of tau pathology are poorly understood. We show here that intracerebral injections of preformed synthetic tau fibrils into the hippocampus or frontal cortex of young tau transgenic mice expressing mutant human P301L tau induces tau hyperphosphorylation and aggregation around the site of injection, as well as a time-dependent propagation of tau pathology to interconnected brain areas distant from the injection site. Furthermore, we show that the tau pathology as a consequence of injection of tau preformed fibrils into the hippocampus induces selective loss of CA1 neurons. Together, our data confirm previous studies on the seeded induction and the spreading of tau pathology in a different tau transgenic mouse model and reveals neuronal loss associated with seeded tau pathology in tau transgenic mouse brain. These results further validate the utility of the tau seeding model in studying disease transmission, and provide a more complete in vivo tauopathy model with associated neurodegeneration which can be used to investigate the mechanisms involved in tau aggregation and spreading, as well as aid in the search for disease modifying treatments for Alzheimer's disease and related tauopathies. PMID:25220759

  14. Reconstruction of {tau}-tilde{sub 1} mass at the LHC

    SciTech Connect

    Djilkibaev, R. M.; Konoplich, R. V.

    2011-01-15

    The cascade mass reconstruction approach was used for mass reconstruction of the lightest {tau}-tilde produced at the LHC in the cascade decay g-tilde {yields} b-tildeb {yields} {chi}-tilde{sub 2}{sup 0}bb {yields} {tau}-tilde{sub 1}{tau}bb {yields} {chi}-tilde{sub 1}{sup 0}{tau}{tau}bb. The {tau}-tilde{sub 1} mass was reconstructed assuming that masses of gluino, bottom squark, and two lightest neutralinos were reconstructed in advance. SUSY data sample sets for the SU(3) model point containing 160k events each were generated which corresponded to an integrated luminosity of about 8 fb{sup -1} at 14 TeV. These events were passed through the AcerDET detector simulator, which parametrized the response of a generic LHC detector. The mass of the {tau}-tilde{sub 1} was reconstructed with a precision of about 20% on average.

  15. On the Behavior of the Effective QCD Coupling {alpha}{sub {tau}}(s)at Low Scales

    SciTech Connect

    Brodsky, Stanley J.

    2002-12-11

    The hadronic decays of the {tau} lepton can be used to determine the effective charge {alpha}{tau}(m{sub {tau}{prime}}{sup 2}) for a hypothetical {tau}-lepton with mass in the range 0 < m{sub {tau}{prime}} < m{sub {tau}}. This definition provides a fundamental definition of the QCD coupling at low mass scales. We study the behavior of {alpha}{sub {tau}} at low mass scales directly from first principles and without any renormalization-scheme dependence by looking at the experimental data from the OPAL Collaboration. The results are consistent with the freezing of the physical coupling at mass scales s = m{sub {tau}{prime}}{sup 2} of order 1 GeV{sup 2} with a magnitude {alpha}{sub {tau}} {approx} 0.9 {+-} 0.1.

  16. FTDP-17 tau mutations decrease the susceptibility of tau to calpain I digestion.

    PubMed

    Yen, S; Easson, C; Nacharaju, P; Hutton, M; Yen, S H

    1999-11-12

    Frontal temporal dementia and Parkinsonism linked to chromosome 17 (FTDP-17) is caused by splice site and missense mutations in the tau gene, and characterized by the accumulation of filamentous tau in cerebral neurons and glia. The missense mutations reduce the ability of tau to promote microtubule assembly and increase the ability of tau to form filaments. In this report we demonstrate that mutants V337M and R406W are less susceptible than mutant P301L or corresponding wild type tau to degradation by calpain I. The differences were at least in part due to changes in accessibility of a cleavage site located about 100 amino acids off the carboxy-terminus. The results suggest that the pathogenesis of some forms of FTDP-17 may involve tau accumulation due to decreased proteolytic degradation. PMID:10561502

  17. Progranulin reduction is associated with increased tau phosphorylation in P301L tau transgenic mice.

    PubMed

    Hosokawa, Masato; Arai, Tetsuaki; Masuda-Suzukake, Masami; Kondo, Hiromi; Matsuwaki, Takashi; Nishihara, Masugi; Hasegawa, Masato; Akiyama, Haruhiko

    2015-02-01

    Granulin (GRN) mutations have been identified in familial frontotemporal lobar degeneration patients with ubiquitin pathology. GRN transcript haploinsufficiency is proposed as a disease mechanism that leads to the loss of functional progranulin (PGRN) protein. Thus, these mutations are strongly involved in frontotemporal lobar degeneration pathogenesis. Moreover, recent findings indicate that GRN mutations are associated with other neurodegenerative disorders with tau pathology, including Alzheimer disease and corticobasal degeneration. To investigate the potential influence of a decline in PGRN protein on tau accumulation, P301L tau transgenic mice were interbred with GRN-deficient mice, producing P301L tau transgenic mice harboring the GRN hemizygote. Brains were collected from 13- and 19-month-old mice, and sequential extraction of proteins, immunoblotting, and immunohistochemical analyses were performed. Immunoblotting analysis revealed that tau phosphorylation was accelerated in the Tris-saline soluble fraction of 13-month-old and in the sarkosyl-insoluble fraction of 19-month-old P301L tau/GRN hemizygotes compared with those in fractions from P301L tau transgenic mice. Activity of cyclin-dependent kinases was also upregulated in the brains of P301L tau/GRN hemizygote mice. Although the mechanisms involved in these findings remain unknown, our data suggest that a reduction in PGRN protein might contribute to phosphorylation and intraneuronal accumulation of tau. PMID:25575133

  18. Anti-tau antibody reduces insoluble tau and decreases brain atrophy

    PubMed Central

    Yanamandra, Kiran; Jiang, Hong; Mahan, Thomas E; Maloney, Susan E; Wozniak, David F; Diamond, Marc I; Holtzman, David M

    2015-01-01

    Objective We previously found a strong reduction in tau pathology and insoluble tau in P301S tau transgenic mice following intracerebroventricular infusion of the anti-tau antibody HJ8.5. We sought to determine the effects of HJ8.5 in the same model following peripheral administration. Methods The primary objective was to determine if HJ8.5 administered at a dose of 50mgkg?1week?1 by intraperitoneal (IP) injection to 6-month-old P301S mice for 3months would influence phospho-tau (p-tau) accumulation, tau insolubility, and neurodegeneration. Results Treatment with HJ8.5 at 50mg/kg showed a very strong decrease in detergent-insoluble tau. Importantly, HJ8.5 significantly reduced the loss of cortical and hippocampal tissue volumes compared to control treated mice. HJ8.5 treatment reduced hippocampal CA1 cellular layer staining with the p-tau antibody AT8 and thio-S-positive tau aggregates in piriform cortex and amygdala. Moreover, mice treated with HJ8.5 at 50mg/kg showed a decrease in motor/sensorimotor deficits compared to vehicle-treated mice. Some effects of HJ8.5, including reduction in brain atrophy, and p-tau immunostaining were also seen with a dose of 10mgkg?1week?1. In BV2-microglial cells, we observed significantly higher uptake of P301S tau aggregates in the presence of HJ8.5. HJ8.5 treatment also resulted in a large dose-dependent increase of tau in the plasma. Interpretation Our results indicate that systemically administered anti-tau antibody HJ8.5 significantly decreases insoluble tau, decreases brain atrophy, and improves motor/sensorimotor function in a mouse model of tauopathy. These data further support the idea that anti-tau antibodies should be further assessed as a potential treatment for tauopathies. PMID:25815354

  19. Vulnerabilities in the Tau Network and the Role of Ultrasensitive Points in Tau Pathophysiology

    PubMed Central

    Yuraszeck, Theresa M.; Neveu, Pierre; Rodriguez-Fernandez, Maria; Robinson, Anne; Kosik, Kenneth S.; Doyle, Francis J.

    2010-01-01

    The multifactorial nature of disease motivates the use of systems-level analyses to understand their pathology. We used a systems biology approach to study tau aggregation, one of the hallmark features of Alzheimer's disease. A mathematical model was constructed to capture the current state of knowledge concerning tau's behavior and interactions in cells. The model was implemented in silico in the form of ordinary differential equations. The identifiability of the model was assessed and parameters were estimated to generate two cellular states: a population of solutions that corresponds to normal tau homeostasis and a population of solutions that displays aggregation-prone behavior. The model of normal tau homeostasis was robust to perturbations, and disturbances in multiple processes were required to achieve an aggregation-prone state. The aggregation-prone state was ultrasensitive to perturbations in diverse subsets of networks. Tau aggregation requires that multiple cellular parameters are set coordinately to a set of values that drive pathological assembly of tau. This model provides a foundation on which to build and increase our understanding of the series of events that lead to tau aggregation and may ultimately be used to identify critical intervention points that can direct the cell away from tau aggregation to aid in the treatment of tau-mediated (or related) aggregation diseases including Alzheimer's. PMID:21085645

  20. Missense tau mutations identified in FTDP-17 have a small effect on tau-microtubule interactions.

    PubMed

    DeTure, M; Ko, L W; Yen, S; Nacharaju, P; Easson, C; Lewis, J; van Slegtenhorst, M; Hutton, M; Yen, S H

    2000-01-17

    Frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17) is a group of related disorders frequently characterized by the formation of tau inclusions in neurons and glial cells. To determine whether the formation of tau inclusions in FTDP-17 results from an alteration in the ability of mutant tau to maintain the microtubule (MT) system, we compared wild type four-repeat tau with three FTDP-17 mutants (P301L, V337M and R406W) for their ability to bind MT, promote MT assembly and bundling. According to in vitro binding and assembly assays, P301L is the only mutant that demonstrates a small, yet significant reduction, in its affinity for MT while both P301L and R406W have a small reduction in their ability to promote tubulin assembly. Based on studies of neuroblastoma and CHO cells transfected with GFP-tagged tau DNA constructs, both mutant and wild type tau transfectants were indistinguishable in the distribution pattern of tau in terms of co-localization with MT and generation of MT bundles. These results suggest that missense mutation of tau gene do not have an immediate impact on the integrity of MT system, and that exposure of affected neurons to additional insults or factors (e.g., aging) may be needed to initiate the formation of tau inclusions in FTDP-17. PMID:10627302

  1. Formation of filamentous tau aggregations in transgenic mice expressing V337M human tau.

    PubMed

    Tanemura, K; Akagi, T; Murayama, M; Kikuchi, N; Murayama, O; Hashikawa, T; Yoshiike, Y; Park, J M; Matsuda, K; Nakao, S; Sun, X; Sato, S; Yamaguchi, H; Takashima, A

    2001-12-01

    Formation of neurofibrillary tangles (NFTs) is the most common feature in several neurodegenerative diseases, including Alzheimer's disease (AD). Here we report the formation of filamentous tau aggregations having a beta-sheet structure in transgenic mice expressing mutant human tau. These mice contain a tau gene with a mutation of the frontotemporal dementia parkinsonism (FTDP-17) type, in which valine is substituted with methionine residue 337. The aggregation of tau in these transgenic mice satisfies all histological criteria used to identify NFTs common to human neurodegenerative diseases. These mice, therefore, provide a preclinical model for the testing of therapeutic drugs for the treatment of neurodegenerative disorders that exhibit NFTs. PMID:11741399

  2. Orbital motions and light curves of young binaries XZ Tau and VY Tau

    NASA Astrophysics Data System (ADS)

    Dodin, A. V.; Emelyanov, N. V.; Zharova, A. V.; Lamzin, S. A.; Malogolovets, E. V.; Roe, J. M.

    2016-01-01

    The results of our speckle interferometric observations of young binaries VY Tau and XZ Tau are presented. For the first time, we found a relative displacement of VY Tau components as well as a preliminary orbit for XZ Tau. It appeared that the orbit is appreciably non-circular and is inclined by i ? 47? from the plane of the sky. It means that the rotation axis of XZ Tau A and the axis of its jet are significantly non-perpendicular to the orbital plane. We found that the average brightness of XZ Tau had been increasing from the beginning of the last century up to the mid-thirties and then it decreased by ? B > 2 mag. The maximal brightness has been reached significantly later on the time of periastron passage. The total brightness of XZ Tau's components varied in a non-regular way from 1970 to 1985 when eruptions of hot gas from XZ Tau A presumably had occurred. In the early nineties the variations became regular following which a chaotic variability had renewed. We also report that a flare activity of VY Tau has resumed after 40 yr pause, parameters of the previous and new flares are similar, and the flares are related with the A component.

  3. Promotion of hyperphosphorylation by frontotemporal dementia tau mutations.

    PubMed

    Alonso, Alejandra del C; Mederlyova, Anna; Novak, Michal; Grundke-Iqbal, Inge; Iqbal, Khalid

    2004-08-13

    Mutations in the tau gene are known to cosegregate with the disease in frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). However, the molecular mechanism by which these mutations might lead to the disease is not understood. Here, we show that four of the FTDP-17 tau mutations, R406W, V337M, G272V, and P301L, result in tau proteins that are more favorable substrates for phosphorylation by brain protein kinases than the wild-type, largest four-repeat protein tau4L and tau4L more than tau3L. In general, at all the sites studied, mutant tau proteins were phosphorylated faster and to a higher extent than tau4L and tau4L > tau3L. The most dramatic difference found was in the rate and level of phosphorylation of tau4L(R406W) at positions Ser-396, Ser-400, Thr-403, and Ser-404. Phosphorylation of this mutant tau was 12 times faster and 400% greater at Ser-396 and less than 30% at Ser-400, Thr-403, and Ser-404 than phosphorylation of tau4L. The mutated tau proteins polymerized into filaments when 4-6 mol of phosphate per mol of tau were incorporated, whereas wild-type tau required approximately 10 mol of phosphate per mol of protein to self-assemble. Mutated and wild-type tau proteins were able to sequester normal tau upon incorporation of approximately 4 mol of phosphate per mol of protein, which was achieved at as early as 30 min of phosphorylation in the case of mutant tau proteins. These findings taken together suggest that the mutations in tau might cause neurodegeneration by making the protein a more favorable substrate for hyperphosphorylation. PMID:15190058

  4. Deletion of endogenous Tau proteins is not detrimental in Drosophila.

    PubMed

    Burnouf, Sylvie; Grönke, Sebastian; Augustin, Hrvoje; Dols, Jacqueline; Gorsky, Marianna Karina; Werner, Jennifer; Kerr, Fiona; Alic, Nazif; Martinez, Pedro; Partridge, Linda

    2016-01-01

    Human Tau (hTau) is a highly soluble and natively unfolded protein that binds to microtubules within neurons. Its dysfunction and aggregation into insoluble paired helical filaments is involved in the pathogenesis of Alzheimer's disease (AD), constituting, together with accumulated β-amyloid (Aβ) peptides, a hallmark of the disease. Deciphering both the loss-of-function and toxic gain-of-function of hTau proteins is crucial to further understand the mechanisms leading to neurodegeneration in AD. As the fruit fly Drosophila melanogaster expresses Tau proteins (dTau) that are homologous to hTau, we aimed to better comprehend dTau functions by generating a specific tau knock-out (KO) fly line using homologous recombination. We observed that the specific removal of endogenous dTau proteins did not lead to overt, macroscopic phenotypes in flies. Indeed, survival, climbing ability and neuronal function were unchanged in tau KO flies. In addition, we did not find any overt positive or negative effect of dTau removal on human Aβ-induced toxicity. Altogether, our results indicate that the absence of dTau proteins has no major functional impact on flies, and suggests that our tau KO strain is a relevant model to further investigate the role of dTau proteins in vivo, thereby giving additional insights into hTau functions. PMID:26976084

  5. Deletion of endogenous Tau proteins is not detrimental in Drosophila

    PubMed Central

    Burnouf, Sylvie; Grönke, Sebastian; Augustin, Hrvoje; Dols, Jacqueline; Gorsky, Marianna Karina; Werner, Jennifer; Kerr, Fiona; Alic, Nazif; Martinez, Pedro; Partridge, Linda

    2016-01-01

    Human Tau (hTau) is a highly soluble and natively unfolded protein that binds to microtubules within neurons. Its dysfunction and aggregation into insoluble paired helical filaments is involved in the pathogenesis of Alzheimer’s disease (AD), constituting, together with accumulated β-amyloid (Aβ) peptides, a hallmark of the disease. Deciphering both the loss-of-function and toxic gain-of-function of hTau proteins is crucial to further understand the mechanisms leading to neurodegeneration in AD. As the fruit fly Drosophila melanogaster expresses Tau proteins (dTau) that are homologous to hTau, we aimed to better comprehend dTau functions by generating a specific tau knock-out (KO) fly line using homologous recombination. We observed that the specific removal of endogenous dTau proteins did not lead to overt, macroscopic phenotypes in flies. Indeed, survival, climbing ability and neuronal function were unchanged in tau KO flies. In addition, we did not find any overt positive or negative effect of dTau removal on human Aβ-induced toxicity. Altogether, our results indicate that the absence of dTau proteins has no major functional impact on flies, and suggests that our tau KO strain is a relevant model to further investigate the role of dTau proteins in vivo, thereby giving additional insights into hTau functions. PMID:26976084

  6. Biochemical Distribution of Tau Protein in Synaptosomal Fraction of Transgenic Mice Expressing Human P301L Tau

    PubMed Central

    Sahara, Naruhiko; Murayama, Miyuki; Higuchi, Makoto; Suhara, Tetsuya; Takashima, Akihiko

    2014-01-01

    Alzheimers disease is a progressive dementia that is characterized by a loss of recent memory. Evidence has accumulated to support the hypothesis that synapses are critical storage sites for memory. However, it is still uncertain whether tau protein is involved in associative memory storage and whether tau is distributed in mature brain synapses. To address this question, we examined the synaptosomal distribution of tau protein in both JNPL3 transgenic mice expressing human P301L tau and non-transgenic littermates. The JNPL3 mouse line is known as one of the mouse models of human tauopathy that develop motor and behavioral deficits with intracellular tau aggregates in the spinal cord and brainstem. The phenotype of disease progression is highly dependent on strain background. In this study, we confirmed that male JNPL3 transgenic mice with C57BL/6J strain background showed neither any sign of motor deficits nor accumulation of hyperphosphorylated tau in the sarkosyl-insoluble fraction until 18?months of age. Subcellular fractionation analysis showed that both mouse tau and human P301L tau were present in the synaptosomal fraction. Those tau proteins were less-phosphorylated than tau in the cytosolic fraction. Human P301L tau was preferentially distributed in the synaptosomal fraction while mouse endogenous tau was more distributed in the cytosolic fraction. Interestingly, a human-specific tau band with phosphorylation at Ser199 and Ser396 was observed in the synaptosomal fraction of JNPL3 mice. This tau was not identical to either tau species in cytosolic fraction or a prominent hyperphosphorylated 64?kDa tau species that was altered to tau pathology. These results suggest that exogenous human P301L tau induces synaptosomal distribution of tau protein with a certain phosphorylation. Regulating the synaptosomal tau level might be a potential target for a therapeutic intervention directed at preventing neurodegeneration. PMID:24653715

  7. Electrochemical detection of anti-tau antibodies binding to tau protein and inhibition of GSK-3?-catalyzed phosphorylation.

    PubMed

    Esteves-Villanueva, Jose O; Martic-Milne, Sanela

    2016-03-01

    Tau protein hyperphosphorylation triggers tau aggregation and its toxicity, leading to neuronal death and cell-to-cell toxicity. Hence, inhibition of protein kinases is a viable tool toward reduction of tau toxicity. By targeting various epitopes of Tau441 protein immobilized on Au surface, the protein kinase inhibition by anti-tau antibodies was measured by surface electrochemistry. The electrochemical impedance spectroscopy was used to measure the charge transfer resistance (Rct) of nonphosphorylated tau-Au film (nTau-Au) and compared with the phosphorylated tau-Au film (pTau-Au). The pTau-Au films were characterized by X-ray photoelectron spectroscopy (XPS) and time-of-flight secondary ion mass spectrometry (TOF-SIMS), which indicated high phosphorus content. The Rct factor was used as the measure of inhibition efficacies by anti-tau antibodies (D8, A10, P262, and Tau46) in addition to antibody formulation intravenous immunoglobulin (IVIG). The Rct factor for pTau-Au in the absence of antibodies was 0.250.08, indicating a dramatic decrease in Rct on phosphorylation. The Rct factors for Tau46 and A10 were 0.570.22 and 0.650.26, respectively, indicating phosphorylation inhibition. All antibodies exhibited similar binding to nTau-Au. The proposed electrochemical assay may be used for detection of other posttranslational modifications. PMID:26706800

  8. Vaccination with Sarkosyl insoluble PHF-tau decrease neurofibrillary tangles formation in aged tau transgenic mouse model: a pilot study.

    PubMed

    Ando, Kunie; Kabova, Anna; Stygelbout, Virginie; Leroy, Karelle; Heraud, Cline; Frdrick, Christelle; Suain, Valrie; Yilmaz, Zehra; Authelet, Michle; Dedecker, Robert; Potier, Marie-Claude; Duyckaerts, Charles; Brion, Jean-Pierre

    2014-01-01

    Active immunization using tau phospho-peptides in tauopathy mouse models has been observed to reduce tau pathology, especially when given prior to the onset of pathology. Since tau aggregates in these models and in human tauopathies are composed of full-length tau with many post-translational modifications, and are composed of several tau isoforms in many of them, pathological tau proteins bearing all these post-translational modifications might prove to be optimal tau conformers to use as immunogens, especially in models with advanced tau pathology. To this aim, we immunized aged wild-type and mutant tau mice with preparations containing human paired helical filaments (PHF) emulsified in Alum-adjuvant. This immunization protocol with fibrillar PHF-tau was well tolerated and did not induce an inflammatory reaction in the brain or adverse effect in these aged mice. Mice immunized with four repeated injections developed anti-PHF-tau antibodies with rising titers that labeled human neurofibrillary tangles in situ. Immunized mutant tau mice had a lower density of hippocampal Gallyas-positive neurons. Brain levels of Sarkosyl-insoluble tau were also reduced in immunized mice. These results indicate that an immunization protocol using fibrillar PHF-tau proteins is an efficient and tolerated approach to reduce tau pathology in an aged tauopathy animal model. PMID:24614899

  9. ATLAS Search for SM H{yields}{tau}{tau} in the VBF Production Mode

    SciTech Connect

    Hanninger, Guilherme Nunes

    2008-11-23

    This article discusses the search for the Standard Model Higgs boson produced in vector boson fusion and subsequent decay into {tau} pairs with the ATLAS detector at the Large Hadron Collider. This analysis is based on Monte Carlo signal and background samples simulated with a detailed detector description and the entire trigger chain. Preliminary results are reported including the expected discovery potential with 30 fb{sup -1} of data as well as the 95% expected signal exclusion with 10 fb{sup -1}.

  10. Rapamycin attenuates the progression of tau pathology in P301S tau transgenic mice.

    PubMed

    Ozcelik, Sefika; Fraser, Graham; Castets, Perrine; Schaeffer, Vronique; Skachokova, Zhiva; Breu, Karin; Clavaguera, Florence; Sinnreich, Michael; Kappos, Ludwig; Goedert, Michel; Tolnay, Markus; Winkler, David Theo

    2013-01-01

    Altered autophagy contributes to the pathogenesis of Alzheimer's disease and other tauopathies, for which curative treatment options are still lacking. We have recently shown that trehalose reduces tau pathology in a tauopathy mouse model by stimulation of autophagy. Here, we studied the effect of the autophagy inducing drug rapamycin on the progression of tau pathology in P301S mutant tau transgenic mice. Rapamycin treatment resulted in a significant reduction in cortical tau tangles, less tau hyperphosphorylation, and lowered levels of insoluble tau in the forebrain. The favourable effect of rapamycin on tau pathology was paralleled by a qualitative reduction in astrogliosis. These effects were visible with early preventive or late treatment. We further noted an accumulation of the autophagy associated proteins p62 and LC3 in aged tangle bearing P301S mice that was lowered upon rapamycin treatment. Thus, rapamycin treatment defers the progression of tau pathology in a tauopathy animal model and autophagy stimulation may constitute a therapeutic approach for patients suffering from tauopathies. PMID:23667480

  11. The future of tau physics and tau-charm detector and factory design

    SciTech Connect

    Perl, M.L.

    1991-02-01

    Future research on the tau lepton requires large statistics, thorough investigation of systematic errors, and direct experimental knowledge of backgrounds. Only a tau-charm factory with a specially designed detector can provide all the experimental conditions to meet these requirements. This paper is a summary of three lectures delivered at the 1991 Lake Louise Winter Institute.

  12. Ultrahigh energy tau neutrino flux regeneration while skimming the Earth

    SciTech Connect

    Bigas, Oscar Blanch

    2008-09-15

    The detection of Earth-skimming tau neutrinos has turned into a very promising strategy for the observation of ultra-high-energy cosmic neutrinos. The sensitivity of this channel crucially depends on the parameters of the propagation of the tau neutrinos through the terrestrial crust, which governs the flux of emerging tau leptons that can be detected. One of the characteristics of this propagation is the possibility of regeneration through multiple {nu}{sub {tau}}{r_reversible}{tau} conversions, which are often neglected in the standard picture. In this paper, we solve the transport equations governing the {nu}{sub {tau}} propagation and compare the flux of emerging tau leptons obtained allowing regeneration or not. We discuss the validity of the approximation of neglecting the {nu}{sub {tau}} regeneration using different scenarios for the neutrino-nucleon cross sections and the tau energy losses.

  13. A Search for supersymmetric Higgs bosons in the di-tau decay mode in p anti-p collisions at s**(1/2) = 1.8-TeV

    SciTech Connect

    Acosta, D.; Affolder, Anthony A.; Albrow, M.G.; Ambrose, D.; Amidei, D.; Anikeev, K.; Antos, J.; Apollinari, G.; Arisawa, T.; Artikov, A.; Ashmanskas, W.; Azfar, F.; Azzi-Bacchetta, P.; Bacchetta, N.; Bachacou, H.; Badgett, W.; Barbaro-Galtieri, A.; Barnes, V.E.; Barnett, B.A.; Baroiant, S.; Barone, M.; /Taiwan, Inst. Phys. /Argonne, PHY /INFN, Bologna /Brandeis U. /UC, Davis /UCLA /UC, Santa Barbara /Cantabria Inst. of Phys. /Cantabria U., Santander /Carnegie Mellon U. /Chicago U., EFI /Chicago U. /Dubna, JINR /Duke U. /Fermilab /Florida U. /Frascati /Geneva U. /Glasgow U. /Harvard U. /Hiroshima U.

    2005-06-01

    A search for direct production of Higgs bosons in the di-tau decay mode is performed with 86.3 {+-} 3.5 pb{sup -1} of data collected with the Collider Detector at Fermilab during the 1994-1995 data taking period of the Tevatron. We search for events where one tau decays to an electron plus neutrinos and the other tau decays hadronically. We perform a counting experiment and set limits on the cross section for supersymmetric Higgs boson production where tan {beta} is large and m{sub A} is small. For a benchmark parameter space point where m{sub A{sup 0}} = 100 GeV/c{sup 2} and tan {beta} = 50, we limit the production cross section multiplied by the branching ratio to be less than 77.9 pb at the 95% confidence level compared to theoretically predicted value of 11.0 pb. This is the first search for Higgs bosons decaying to tau pairs at a hadron collider.

  14. Search for Pair Production of Scalar Top Quarks Decaying to a tau Lepton and a b Quark in ppbar Collisions at sqrt{s}=1.96 TeV

    SciTech Connect

    Brigliadori, L.; Zheng, Y.; Zucchelli, S.; /Taiwan, Inst. Phys. /Bologna U. /Argonne /Barcelona, IFAE /Baylor U., Math. Dept. /Bologna U. /Brandeis U. /UC, Davis /UCLA /UC, San Diego /UC, Santa Barbara /Cantabria U., Santander /Carnegie Mellon U.

    2008-02-01

    We present the results of a search for pair production of scalar top quarks ({tilde t}{sub 1}) in an R-parity violating supersymmetric scenario using 322 pb{sup -1} of p{bar p} collisions at {radical}s = 1.96 TeV collected by the upgraded Collider Detector at Fermilab. We assume each {tilde t}{sub 1} decays into a {tau} lepton and a b quark with a branching ratio {beta}, and that the final state contains either an electron or a muon from a leptonic {tau} decay, a hadronically decaying {tau} lepton, and two or more jets. Two candidate events pass our final selection criteria, consistent with the expectation from standard model processes. We present upper limits on the cross section times branching ratio squared {sigma}({tilde t}{sub 1}{bar {tilde t}}{sub 1}) x {beta}{sup 2} as a function of the stop mass m({tilde t}{sub 1}). Assuming {beta} = 1, we set a 95% confidence level limit m({tilde t}{sub 1}) > 153 GeV=c{sup 2} obtained using a next-to-leading order cross section. These limits are also fully applicable to the case of a pair produced third generation scalar leptoquark decaying into a {tau} lepton and a b quark.

  15. Passive immunization with phospho-tau antibodies reduces tau pathology and functional deficits in two distinct mouse tauopathy models.

    PubMed

    Sankaranarayanan, Sethu; Barten, Donna M; Vana, Laurel; Devidze, Nino; Yang, Ling; Cadelina, Gregory; Hoque, Nina; DeCarr, Lynn; Keenan, Stefanie; Lin, Alan; Cao, Yang; Snyder, Bradley; Zhang, Bin; Nitla, Magdalena; Hirschfeld, Gregg; Barrezueta, Nestor; Polson, Craig; Wes, Paul; Rangan, Vangipuram S; Cacace, Angela; Albright, Charles F; Meredith, Jere; Trojanowski, John Q; Lee, Virginia M-Y; Brunden, Kurt R; Ahlijanian, Michael

    2015-01-01

    In Alzheimer's disease (AD), an extensive accumulation of extracellular amyloid plaques and intraneuronal tau tangles, along with neuronal loss, is evident in distinct brain regions. Staging of tau pathology by postmortem analysis of AD subjects suggests a sequence of initiation and subsequent spread of neurofibrillary tau tangles along defined brain anatomical pathways. Further, the severity of cognitive deficits correlates with the degree and extent of tau pathology. In this study, we demonstrate that phospho-tau (p-tau) antibodies, PHF6 and PHF13, can prevent the induction of tau pathology in primary neuron cultures. The impact of passive immunotherapy on the formation and spread of tau pathology, as well as functional deficits, was subsequently evaluated with these antibodies in two distinct transgenic mouse tauopathy models. The rTg4510 transgenic mouse is characterized by inducible over-expression of P301L mutant tau, and exhibits robust age-dependent brain tau pathology. Systemic treatment with PHF6 and PHF13 from 3 to 6 months of age led to a significant decline in brain and CSF p-tau levels. In a second model, injection of preformed tau fibrils (PFFs) comprised of recombinant tau protein encompassing the microtubule-repeat domains into the cortex and hippocampus of young P301S mutant tau over-expressing mice (PS19) led to robust tau pathology on the ipsilateral side with evidence of spread to distant sites, including the contralateral hippocampus and bilateral entorhinal cortex 4 weeks post-injection. Systemic treatment with PHF13 led to a significant decline in the spread of tau pathology in this model. The reduction in tau species after p-tau antibody treatment was associated with an improvement in novel-object recognition memory test in both models. These studies provide evidence supporting the use of tau immunotherapy as a potential treatment option for AD and other tauopathies. PMID:25933020

  16. Passive Immunization with Phospho-Tau Antibodies Reduces Tau Pathology and Functional Deficits in Two Distinct Mouse Tauopathy Models

    PubMed Central

    Sankaranarayanan, Sethu; Barten, Donna M.; Vana, Laurel; Devidze, Nino; Yang, Ling; Cadelina, Gregory; Hoque, Nina; DeCarr, Lynn; Keenan, Stefanie; Lin, Alan; Cao, Yang; Snyder, Bradley; Zhang, Bin; Nitla, Magdalena; Hirschfeld, Gregg; Barrezueta, Nestor; Polson, Craig; Wes, Paul; Rangan, Vangipuram S.; Cacace, Angela; Albright, Charles F.; Meredith, Jere; Trojanowski, John Q.; Lee, Virginia M-Y.; Brunden, Kurt R.; Ahlijanian, Michael

    2015-01-01

    In Alzheimer’s disease (AD), an extensive accumulation of extracellular amyloid plaques and intraneuronal tau tangles, along with neuronal loss, is evident in distinct brain regions. Staging of tau pathology by postmortem analysis of AD subjects suggests a sequence of initiation and subsequent spread of neurofibrillary tau tangles along defined brain anatomical pathways. Further, the severity of cognitive deficits correlates with the degree and extent of tau pathology. In this study, we demonstrate that phospho-tau (p-tau) antibodies, PHF6 and PHF13, can prevent the induction of tau pathology in primary neuron cultures. The impact of passive immunotherapy on the formation and spread of tau pathology, as well as functional deficits, was subsequently evaluated with these antibodies in two distinct transgenic mouse tauopathy models. The rTg4510 transgenic mouse is characterized by inducible over-expression of P301L mutant tau, and exhibits robust age-dependent brain tau pathology. Systemic treatment with PHF6 and PHF13 from 3 to 6 months of age led to a significant decline in brain and CSF p-tau levels. In a second model, injection of preformed tau fibrils (PFFs) comprised of recombinant tau protein encompassing the microtubule-repeat domains into the cortex and hippocampus of young P301S mutant tau over-expressing mice (PS19) led to robust tau pathology on the ipsilateral side with evidence of spread to distant sites, including the contralateral hippocampus and bilateral entorhinal cortex 4 weeks post-injection. Systemic treatment with PHF13 led to a significant decline in the spread of tau pathology in this model. The reduction in tau species after p-tau antibody treatment was associated with an improvement in novel-object recognition memory test in both models. These studies provide evidence supporting the use of tau immunotherapy as a potential treatment option for AD and other tauopathies. PMID:25933020

  17. Curcumin improves tau-induced neuronal dysfunction of nematodes.

    PubMed

    Miyasaka, Tomohiro; Xie, Ce; Yoshimura, Satomi; Shinzaki, Yuki; Yoshina, Sawako; Kage-Nakadai, Eriko; Mitani, Shohei; Ihara, Yasuo

    2016-03-01

    Tau is a key protein in the pathogenesis of various neurodegenerative diseases, which are categorized as tauopathies. Because the extent of tau pathologies is closely linked to that of neuronal loss and the clinical symptoms in Alzheimer's disease, anti-tau therapeutics, if any, could be beneficial to a broad spectrum of tauopathies. To learn more about tauopathy, we developed a novel transgenic nematode (Caenorhabditis elegans) model that expresses either wild-type or R406W tau in all the neurons. The wild-type tau-expressing worms exhibited uncoordinated movement (Unc) and neuritic abnormalities. Tau accumulated in abnormal neurites that lost microtubules. Similar abnormalities were found in the worms that expressed low levels of R406W-tau but were not in those expressing comparative levels of wild-type tau. Biochemical studies revealed that tau is aberrantly phosphorylated but forms no detergent-insoluble aggregates. Drug screening performed in these worms identified curcumin, a major phytochemical compound in turmeric, as a compound that reduces not only Unc but also the neuritic abnormalities in both wild-type and R406W tau-expressing worms. Our observations suggest that microtubule stabilization mediates the antitoxicity effect of curcumin. Curcumin is also effective in the worms expressing tau fragment, although it does not prevent the formation of tau-fragment dimers. These data indicate that curcumin improves the tau-induced neuronal dysfunction that is independent of insoluble aggregates of tau. PMID:26923403

  18. Trehalose ameliorates dopaminergic and tau pathology in parkin deleted/tau overexpressing mice through autophagy activation.

    PubMed

    Rodrguez-Navarro, Jose A; Rodrguez, Laura; Casarejos, Mara J; Solano, Rosa M; Gmez, Ana; Perucho, Juan; Cuervo, Ana Mara; Garca de Ybenes, Justo; Mena, Mara A

    2010-09-01

    Tauopathies are neurodegenerative diseases, sporadic or familial, mainly characterized by dementia and parkinsonism associated to atrophy of the frontotemporal cortex and the basal ganglia, with deposition of abnormal tau in brain. Hereditary tauopathies are related with mutations of the tau gene. Up to the present, these diseases have not been helped by any disease-modifying treatment, and patients die a few years after the onset of symptoms. We have developed and characterized a mouse model of tauopathy with parkinsonism, overexpressing human mutated tau protein with deletion of parkin (PK(-/-)/Tau(VLW)). At 3 months of age, these mice present abnormal dopamine-related behavior, severe dropout of dopamine neurons in the ventral midbrain, reduced dopamine levels in the striatum and abundant phosphorylated tau-positive neuritic plaques, neurofibrillary tangles, astrogliosis, and, at 12 months old, plaques of murine beta-amyloid in the hippocampus. Trehalose is a natural disaccharide that increases the removal of abnormal proteins through enhancement of autophagy. In this work, we tested if 1% trehalose in the drinking water reverts the PK(-/-)/Tau(VLW) phenotype. The treatment with trehalose of 3-month-old PK(-/-)/Tau(VLW) mice for 2.5 months reverted the dropout of dopamine neurons, which takes place in the ventral midbrain of vehicle treated PK(-/-)/Tau(VLW) and the reduced dopamine-related proteins levels in the midbrain and striatum. The number of phosphorylated tau-positive neuritic plaques and the levels of phosphorylated tau decreased, as well as astrogliosis in brain regions. The autophagy markers in the brain, the autophagic vacuoles isolated from the liver, and the electron microscopy data indicate that these effects of trehalose are mediated by autophagy. The treatment with trehalose for 4 months of 3-month-old PK(-/-)/Tau(VLW) mice maintained the amelioration of the tau pathology and astrogliosis but failed to revert DA-related pathology in the striatum. Furthermore, the 3-week treatment with trehalose of 14-month-old PK(-/-)/Tau(VLW) mice, at the limit of their life expectancy, improved the motor behavior and anxiety of these animals, and reduced their levels of phosphorylated tau and the number of murine beta-amyloid plaques. Trehalose is neuroprotective in this model of tauopathy. Since trehalose is free of toxic effects at high concentrations, this study opens the way for clinical studies of the effects of trehalose in human tauopathies. PMID:20546895

  19. Neurodegeneration with tau accumulation in a transgenic mouse expressing V337M human tau.

    PubMed

    Tanemura, Kentaro; Murayama, Miyuki; Akagi, Takumi; Hashikawa, Tsutomu; Tominaga, Takashi; Ichikawa, Michinori; Yamaguchi, Haruyasu; Takashima, Akihiko

    2002-01-01

    Formation of neurofibrillary tangles (NFTs) is a common neuropathological feature found in several neurodegenerative diseases, including Alzheimer's disease. We have developed a transgenic (Tg) mouse expressing mutant human tau (V337M), derived from frontotemporal dementia parkinsonism-17. V337M Tg mice revealed tau aggregations in the hippocampus, which fulfills the histological criteria for NFTs in human neurodegenerative diseases. Concurrent with the accumulation of RNA and phosphorylated tau, neurons exhibited morphological characteristics of degenerating neurons, which include a loss of microtubules, accumulation of ribosomes, plasma and nuclear membrane ruffling, and swelling of the Golgi network. Thus, mutant tau induces neuronal degeneration associated with the accumulation of RNA and phosphorylated tau. The functional consequences of this neuronal degeneration was evidenced by the reduction of hippocampal neural activity and behavioral abnormality in Tg mice. PMID:11756496

  20. Search for neutral Higgs bosons of the minimal supersymmetric standard model decaying to tau pairs in pp collisions at square root of s = 1.96 TeV.

    PubMed

    Abulencia, A; Acosta, D; Adelman, J; Affolder, T; Akimoto, T; Albrow, M G; Ambrose, D; Amerio, S; Amidei, D; Anastassov, A; Anikeev, K; Annovi, A; Antos, J; Aoki, M; Apollinari, G; Arguin, J-F; Arisawa, T; Artikov, A; Ashmanskas, W; Attal, A; Azfar, F; Azzi-Bacchetta, P; Azzurri, P; Bacchetta, N; Bachacou, H; Badgett, W; Barbaro-Galtieri, A; Barnes, V E; Barnett, B A; Baroiant, S; Bartsch, V; Bauer, G; Bedeschi, F; Behari, S; Belforte, S; Bellettini, G; Bellinger, J; Belloni, A; Ben-Haim, E; Benjamin, D; Beretvas, A; Beringer, J; Berry, T; Bhatti, A; Binkley, M; Bisello, D; Bishai, M; Blair, R E; Blocker, C; Bloom, K; Blumenfeld, B; Bocci, A; Bodek, A; Boisvert, V; Bolla, G; Bolshov, A; Bortoletto, D; Boudreau, J; Bourov, S; Boveia, A; Brau, B; Bromberg, C; Brubaker, E; Budagov, J; Budd, H S; Budd, S; Burkett, K; Busetto, G; Bussey, P; Byrum, K L; Cabrera, S; Campanelli, M; Campbell, M; Canelli, F; Canepa, A; Carlsmith, D; Carosi, R; Carron, S; Casarsa, M; Castro, A; Catastini, P; Cauz, D; Cavalli-Sforza, M; Cerri, A; Cerrito, L; Chang, S H; Chapman, J; Chen, Y C; Chertok, M; Chiarelli, G; Chlachidze, G; Chlebana, F; Cho, I; Cho, K; Chokheli, D; Chou, J P; Chu, P H; Chuang, S H; Chung, K; Chung, W H; Chung, Y S; Ciljak, M; Ciobanu, C I; Ciocci, M A; Clark, A; Clark, D; Coca, M; Connolly, A; Convery, M E; Conway, J; Cooper, B; Copic, K; Cordelli, M; Cortiana, G; Cruz, A; Cuevas, J; Culbertson, R; Cyr, D; Daronco, S; D'Auria, S; D'onofrio, M; Dagenhart, D; de Barbaro, P; De Cecco, S; Deisher, A; De Lentdecker, G; Dell'Orso, M; Demers, S; Demortier, L; Deng, J; Deninno, M; De Pedis, D; Derwent, P F; Dionisi, C; Dittmann, J; Dituro, P; Drr, C; Dominguez, A; Donati, S; Donega, M; Dong, P; Donini, J; Dorigo, T; Dube, S; Ebina, K; Efron, J; Ehlers, J; Erbacher, R; Errede, D; Errede, S; Eusebi, R; Fang, H C; Farrington, S; Fedorko, I; Fedorko, W T; Feild, R G; Feindt, M; Fernandez, J P; Field, R; Flanagan, G; Flores-Castillo, L R; Foland, A; Forrester, S; Foster, G W; Franklin, M; Freeman, J C; Fujii, Y; Furic, I; Gajjar, A; Gallinaro, M; Galyardt, J; Garcia, J E; Garcia Sciveres, M; Garfinkel, A F; Gay, C; Gerberich, H; Gerchtein, E; Gerdes, D; Giagu, S; Giannetti, P; Gibson, A; Gibson, K; Ginsburg, C; Giolo, K; Giordani, M; Giunta, M; Giurgiu, G; Glagolev, V; Glenzinski, D; Gold, M; Goldschmidt, N; Goldstein, J; Gomez, G; Gomez-Ceballos, G; Goncharov, M; Gonzlez, O; Gorelov, I; Goshaw, A T; Gotra, Y; Goulianos, K; Gresele, A; Griffiths, M; Grinstein, S; Grosso-Pilcher, C; Grundler, U; Guimaraes da Costa, J; Haber, C; Hahn, S R; Hahn, K; Halkiadakis, E; Hamilton, A; Han, B-Y; Handler, R; Happacher, F; Hara, K; Hare, M; Harper, S; Harr, R F; Harris, R M; Hatakeyama, K; Hauser, J; Hays, C; Hayward, H; Heijboer, A; Heinemann, B; Heinrich, J; Hennecke, M; Herndon, M; Heuser, J; Hidas, D; Hill, C S; Hirschbuehl, D; Hocker, A; Holloway, A; Hou, S; Houlden, M; Hsu, S-C; Huffman, B T; Hughes, R E; Huston, J; Ikado, K; Incandela, J; Introzzi, G; Iori, M; Ishizawa, Y; Ivanov, A; Iyutin, B; James, E; Jang, D; Jayatilaka, B; Jeans, D; Jensen, H; Jeon, E J; Jones, M; Joo, K K; Jun, S Y; Junk, T R; Kamon, T; Kang, J; Karagoz-Unel, M; Karchin, P E; Kato, Y; Kemp, Y; Kephart, R; Kerzel, U; Khotilovich, V; Kilminster, B; Kim, D H; Kim, H S; Kim, J E; Kim, M J; Kim, M S; Kim, S B; Kim, S H; Kim, Y K; Kirby, M; Kirsch, L; Klimenko, S; Klute, M; Knuteson, B; Ko, B R; Kobayashi, H; Kondo, K; Kong, D J; Konigsberg, J; Kordas, K; Korytov, A; Kotwal, A V; Kovalev, A; Kraus, J; Kravchenko, I; Kreps, M; Kreymer, A; Kroll, J; Krumnack, N; Kruse, M; Krutelyov, V; Kuhlmann, S E; Kusakabe, Y; Kwang, S; Laasanen, A T; Lai, S; Lami, S; Lammel, S; Lancaster, M; Lander, R L; Lannon, K; Lath, A; Latino, G; Lazzizzera, I; Lecci, C; Lecompte, T; Lee, J; Lee, J; Lee, S W; Lefvre, R; Leonardo, N; Leone, S; Levy, S; Lewis, J D; Li, K; Lin, C; Lin, C S; Lindgren, M; Lipeles, E; Liss, T M; Lister, A; Litvintsev, D O; Liu, T; Liu, Y; Lockyer, N S; Loginov, A; Loreti, M; Loverre, P; Lu, R-S; Lucchesi, D; Lujan, P; Lukens, P; Lungu, G; Lyons, L; Lys, J; Lysak, R; Lytken, E; Mack, P; Macqueen, D; Madrak, R; Maeshima, K; Maksimovic, P; Manca, G; Margaroli, F; Marginean, R; Marino, C; Martin, A; Martin, M; Martin, V; Martnez, M; Maruyama, T; Matsunaga, H; Mattson, M E; Mazini, R; Mazzanti, P; McFarland, K S; McGivern, D; McIntyre, P; McNamara, P; McNulty, R; Mehta, A; Menzemer, S; Menzione, A; Merkel, P; Mesropian, C; Messina, A; von der Mey, M; Miao, T; Miladinovic, N; Miles, J; Miller, R; Miller, J S; Mills, C; Milnik, M; Miquel, R; Miscetti, S; Mitselmakher, G; Miyamoto, A; Moggi, N; Mohr, B; Moore, R; Morello, M; Movilla Fernandez, P; Mlmenstdt, J; Mukherjee, A; Mulhearn, M; Muller, Th; Mumford, R; Murat, P; Nachtman, J; Nahn, S; Nakano, I; Napier, A; Naumov, D; Necula, V; Neu, C; Neubauer, M S; Nielsen, J; Nigmanov, T; Nodulman, L; Norniella, O; Ogawa, T

    2006-01-13

    We present a search for neutral supersymmetric Higgs bosons decaying to tau pairs produced in pp collisions at square root of s = 1.96 TeV. The data, corresponding to 310 pb(-1) integrated luminosity, were collected with the Collider Detector at Fermilab in run II of the Tevatron. No significant excess above the standard model backgrounds is observed. We set exclusion limits on the production cross section times branching fraction to tau pairs for Higgs boson masses in the range from 90 to 250 GeV/c2. PMID:16486438

  1. Search for W‧ decaying to tau lepton and neutrino in proton-proton collisions at √{ s} = 8 TeV

    NASA Astrophysics Data System (ADS)

    Khachatryan, V.; Sirunyan, A. M.; Tumasyan, A.; Adam, W.; Asilar, E.; Bergauer, T.; Brandstetter, J.; Brondolin, E.; Dragicevic, M.; Erö, J.; Flechl, M.; Friedl, M.; Frühwirth, R.; Ghete, V. M.; Hartl, C.; Hörmann, N.; Hrubec, J.; Jeitler, M.; Knünz, V.; König, A.; Krammer, M.; Krätschmer, I.; Liko, D.; Matsushita, T.; Mikulec, I.; Rabady, D.; Rahbaran, B.; Rohringer, H.; Schieck, J.; Schöfbeck, R.; Strauss, J.; Treberer-Treberspurg, W.; Waltenberger, W.; Wulz, C.-E.; Mossolov, V.; Shumeiko, N.; Suarez Gonzalez, J.; Alderweireldt, S.; Cornelis, T.; de Wolf, E. A.; Janssen, X.; Knutsson, A.; Lauwers, J.; Luyckx, S.; Ochesanu, S.; Rougny, R.; van de Klundert, M.; van Haevermaet, H.; van Mechelen, P.; van Remortel, N.; van Spilbeeck, A.; Abu Zeid, S.; Blekman, F.; D'Hondt, J.; Daci, N.; de Bruyn, I.; Deroover, K.; Heracleous, N.; Keaveney, J.; Lowette, S.; Moreels, L.; Olbrechts, A.; Python, Q.; Strom, D.; Tavernier, S.; van Doninck, W.; van Mulders, P.; van Onsem, G. P.; van Parijs, I.; Barria, P.; Caillol, C.; Clerbaux, B.; de Lentdecker, G.; Delannoy, H.; Fasanella, G.; Favart, L.; Gay, A. P. R.; Grebenyuk, A.; Lenzi, T.; Léonard, A.; Maerschalk, T.; Marinov, A.; Perniè, L.; Randle-Conde, A.; Reis, T.; Seva, T.; Vander Velde, C.; Vanlaer, P.; Yonamine, R.; Zenoni, F.; Zhang, F.; Beernaert, K.; Benucci, L.; Cimmino, A.; Crucy, S.; Dobur, D.; Fagot, A.; Garcia, G.; Gul, M.; McCartin, J.; Ocampo Rios, A. A.; Poyraz, D.; Ryckbosch, D.; Salva, S.; Sigamani, M.; Strobbe, N.; Tytgat, M.; van Driessche, W.; Yazgan, E.; Zaganidis, N.; Basegmez, S.; Beluffi, C.; Bondu, O.; Brochet, S.; Bruno, G.; Castello, R.; Caudron, A.; Ceard, L.; da Silveira, G. G.; Delaere, C.; Favart, D.; Forthomme, L.; Giammanco, A.; Hollar, J.; Jafari, A.; Jez, P.; Komm, M.; Lemaitre, V.; Mertens, A.; Nuttens, C.; Perrini, L.; Pin, A.; Piotrzkowski, K.; Popov, A.; Quertenmont, L.; Selvaggi, M.; Vidal Marono, M.; Beliy, N.; Hammad, G. H.; Aldá Júnior, W. L.; Alves, G. A.; Brito, L.; Correa Martins Junior, M.; Hensel, C.; Mora Herrera, C.; Moraes, A.; Pol, M. E.; Rebello Teles, P.; Belchior Batista Das Chagas, E.; Carvalho, W.; Chinellato, J.; Custódio, A.; da Costa, E. M.; de Jesus Damiao, D.; de Oliveira Martins, C.; Fonseca de Souza, S.; Huertas Guativa, L. M.; Malbouisson, H.; Matos Figueiredo, D.; Mundim, L.; Nogima, H.; Prado da Silva, W. L.; Santoro, A.; Sznajder, A.; Tonelli Manganote, E. J.; Vilela Pereira, A.; Ahuja, S.; Bernardes, C. A.; de Souza Santos, A.; Dogra, S.; Fernandez Perez Tomei, T. R.; Gregores, E. M.; Mercadante, P. G.; Moon, C. S.; Novaes, S. F.; Padula, Sandra S.; Romero Abad, D.; Ruiz Vargas, J. C.; Aleksandrov, A.; Genchev, V.; Hadjiiska, R.; Iaydjiev, P.; Piperov, S.; Rodozov, M.; Stoykova, S.; Sultanov, G.; Vutova, M.; Dimitrov, A.; Glushkov, I.; Litov, L.; Pavlov, B.; Petkov, P.; Ahmad, M.; Bian, J. G.; Chen, G. M.; Chen, H. S.; Chen, M.; Cheng, T.; Du, R.; Jiang, C. H.; Plestina, R.; Romeo, F.; Shaheen, S. M.; Tao, J.; Wang, C.; Wang, Z.; Zhang, H.; Asawatangtrakuldee, C.; Ban, Y.; Li, Q.; Liu, S.; Mao, Y.; Qian, S. J.; Wang, D.; Xu, Z.; Zou, W.; Avila, C.; Cabrera, A.; Chaparro Sierra, L. F.; Florez, C.; Gomez, J. P.; Gomez Moreno, B.; Sanabria, J. C.; Godinovic, N.; Lelas, D.; Polic, D.; Puljak, I.; Ribeiro Cipriano, P. M.; Antunovic, Z.; Kovac, M.; Brigljevic, V.; Kadija, K.; Luetic, J.; Micanovic, S.; Sudic, L.; Attikis, A.; Mavromanolakis, G.; Mousa, J.; Nicolaou, C.; Ptochos, F.; Razis, P. A.; Rykaczewski, H.; Bodlak, M.; Finger, M.; Finger, M.; Assran, Y.; Elgammal, S.; Mahmoud, M. A.; Calpas, B.; Kadastik, M.; Murumaa, M.; Raidal, M.; Tiko, A.; Veelken, C.; Eerola, P.; Pekkanen, J.; Voutilainen, M.; Härkönen, J.; Karimäki, V.; Kinnunen, R.; Lampén, T.; Lassila-Perini, K.; Lehti, S.; Lindén, T.; Luukka, P.; Mäenpää, T.; Peltola, T.; Tuominen, E.; Tuominiemi, J.; Tuovinen, E.; Wendland, L.; Talvitie, J.; Tuuva, T.; Besancon, M.; Couderc, F.; Dejardin, M.; Denegri, D.; Fabbro, B.; Faure, J. L.; Favaro, C.; Ferri, F.; Ganjour, S.; Givernaud, A.; Gras, P.; Hamel de Monchenault, G.; Jarry, P.; Locci, E.; Machet, M.; Malcles, J.; Rander, J.; Rosowsky, A.; Titov, M.; Zghiche, A.; Antropov, I.; Baffioni, S.; Beaudette, F.; Busson, P.; Cadamuro, L.; Chapon, E.; Charlot, C.; Dahms, T.; Davignon, O.; Filipovic, N.; Florent, A.; Granier de Cassagnac, R.; Lisniak, S.; Mastrolorenzo, L.; Miné, P.; Naranjo, I. N.; Nguyen, M.; Ochando, C.; Ortona, G.; Paganini, P.; Regnard, S.; Salerno, R.; Sauvan, J. B.; Sirois, Y.; Strebler, T.; Yilmaz, Y.; Zabi, A.; Agram, J.-L.; Andrea, J.; Aubin, A.; Bloch, D.; Brom, J.-M.; Buttignol, M.; Chabert, E. C.; Chanon, N.; Collard, C.; Conte, E.; Coubez, X.; Fontaine, J.-C.; Gelé, D.; Goerlach, U.; Goetzmann, C.; Le Bihan, A.-C.; Merlin, J. A.; Skovpen, K.; van Hove, P.; Gadrat, S.; Beauceron, S.; Bernet, C.; Boudoul, G.; Bouvier, E.; Carrillo Montoya, C. A.; Chasserat, J.; Chierici, R.; Contardo, D.; Courbon, B.; Depasse, P.; El Mamouni, H.; Fan, J.; Fay, J.; Gascon, S.; Gouzevitch, M.; Ille, B.; Lagarde, F.; Laktineh, I. B.; Lethuillier, M.; Mirabito, L.; Pequegnot, A. L.; Perries, S.; Ruiz Alvarez, J. D.; Sabes, D.; Sgandurra, L.; Sordini, V.; Vander Donckt, M.; Verdier, P.; Viret, S.; Xiao, H.; Toriashvili, T.; Tsamalaidze, Z.; Autermann, C.; Beranek, S.; Edelhoff, M.; Feld, L.; Heister, A.; Kiesel, M. K.; Klein, K.; Lipinski, M.; Ostapchuk, A.; Preuten, M.; Raupach, F.; Schael, S.; Schulte, J. F.; Verlage, T.; Weber, H.; Wittmer, B.; Zhukov, V.; Ata, M.; Brodski, M.; Dietz-Laursonn, E.; Duchardt, D.; Edelhäuser, L.; Endres, M.; Erdmann, M.; Erdweg, S.; Esch, T.; Fischer, R.; Güth, A.; Hebbeker, T.; Heidemann, C.; Hoepfner, K.; Klingebiel, D.; Knochel, A.; Knutzen, S.; Kreuzer, P.; Merschmeyer, M.; Meyer, A.; Millet, P.; Olschewski, M.; Padeken, K.; Papacz, P.; Pook, T.; Radziej, M.; Reithler, H.; Rieger, M.; Scheuch, F.; Sonnenschein, L.; Teyssier, D.; Thüer, S.; Cherepanov, V.; Erdogan, Y.; Flügge, G.; Geenen, H.; Geisler, M.; Hoehle, F.; Kargoll, B.; Kress, T.; Kuessel, Y.; Künsken, A.; Lingemann, J.; Nehrkorn, A.; Nowack, A.; Nugent, I. M.; Pistone, C.; Pooth, O.; Stahl, A.; Aldaya Martin, M.; Asin, I.; Bartosik, N.; Behnke, O.; Behrens, U.; Bell, A. J.; Borras, K.; Burgmeier, A.; Cakir, A.; Calligaris, L.; Campbell, A.; Choudhury, S.; Costanza, F.; Diez Pardos, C.; Dolinska, G.; Dooling, S.; Dorland, T.; Eckerlin, G.; Eckstein, D.; Eichhorn, T.; Flucke, G.; Gallo, E.; Garay Garcia, J.; Geiser, A.; Gizhko, A.; Gunnellini, P.; Hauk, J.; Hempel, M.; Jung, H.; Kalogeropoulos, A.; Karacheban, O.; Kasemann, M.; Katsas, P.; Kieseler, J.; Kleinwort, C.; Korol, I.; Lange, W.; Leonard, J.; Lipka, K.; Lobanov, A.; Lohmann, W.; Mankel, R.; Marfin, I.; Melzer-Pellmann, I.-A.; Meyer, A. B.; Mittag, G.; Mnich, J.; Mussgiller, A.; Naumann-Emme, S.; Nayak, A.; Ntomari, E.; Perrey, H.; Pitzl, D.; Placakyte, R.; Raspereza, A.; Roland, B.; Sahin, M. Ö.; Saxena, P.; Schoerner-Sadenius, T.; Schröder, M.; Seitz, C.; Spannagel, S.; Trippkewitz, K. D.; Walsh, R.; Wissing, C.; Blobel, V.; Centis Vignali, M.; Draeger, A. R.; Erfle, J.; Garutti, E.; Goebel, K.; Gonzalez, D.; Görner, M.; Haller, J.; Hoffmann, M.; Höing, R. S.; Junkes, A.; Klanner, R.; Kogler, R.; Lapsien, T.; Lenz, T.; Marchesini, I.; Marconi, D.; Nowatschin, D.; Ott, J.; Pantaleo, F.; Peiffer, T.; Perieanu, A.; Pietsch, N.; Poehlsen, J.; Rathjens, D.; Sander, C.; Schettler, H.; Schleper, P.; Schlieckau, E.; Schmidt, A.; Schwandt, J.; Seidel, M.; Sola, V.; Stadie, H.; Steinbrück, G.; Tholen, H.; Troendle, D.; Usai, E.; Vanelderen, L.; Vanhoefer, A.; Akbiyik, M.; Barth, C.; Baus, C.; Berger, J.; Böser, C.; Butz, E.; Chwalek, T.; Colombo, F.; de Boer, W.; Descroix, A.; Dierlamm, A.; Fink, S.; Frensch, F.; Giffels, M.; Gilbert, A.; Hartmann, F.; Heindl, S. M.; Husemann, U.; Kassel, F.; Katkov, I.; Kornmayer, A.; Lobelle Pardo, P.; Maier, B.; Mildner, H.; Mozer, M. U.; Müller, T.; Müller, Th.; Plagge, M.; Quast, G.; Rabbertz, K.; Röcker, S.; Roscher, F.; Simonis, H. J.; Stober, F. M.; Ulrich, R.; Wagner-Kuhr, J.; Wayand, S.; Weber, M.; Weiler, T.; Wöhrmann, C.; Wolf, R.; Anagnostou, G.; Daskalakis, G.; Geralis, T.; Giakoumopoulou, V. A.; Kyriakis, A.; Loukas, D.; Psallidas, A.; Topsis-Giotis, I.; Agapitos, A.; Kesisoglou, S.; Panagiotou, A.; Saoulidou, N.; Tziaferi, E.; Evangelou, I.; Flouris, G.; Foudas, C.; Kokkas, P.; Loukas, N.; Manthos, N.; Papadopoulos, I.; Paradas, E.; Strologas, J.; Bencze, G.; Hajdu, C.; Hazi, A.; Hidas, P.; Horvath, D.; Sikler, F.; Veszpremi, V.; Vesztergombi, G.; Zsigmond, A. J.; Beni, N.; Czellar, S.; Karancsi, J.; Molnar, J.; Szillasi, Z.; Bartók, M.; Makovec, A.; Raics, P.; Trocsanyi, Z. L.; Ujvari, B.; Mal, P.; Mandal, K.; Sahoo, N.; Swain, S. K.; Bansal, S.; Beri, S. B.; Bhatnagar, V.; Chawla, R.; Gupta, R.; Bhawandeep, U.; Kalsi, A. K.; Kaur, A.; Kaur, M.; Kumar, R.; Mehta, A.; Mittal, M.; Singh, J. B.; Walia, G.; Kumar, Ashok; Kumar, Arun; Bhardwaj, A.; Choudhary, B. C.; Garg, R. B.; Kumar, A.; Malhotra, S.; Naimuddin, M.; Nishu, N.; Ranjan, K.; Sharma, R.; Sharma, V.; Banerjee, S.; Bhattacharya, S.; Chatterjee, K.; Dey, S.; Dutta, S.; Jain, Sa.; Majumdar, N.; Modak, A.; Mondal, K.; Mukherjee, S.; Mukhopadhyay, S.; Roy, A.; Roy, D.; Roy Chowdhury, S.; Sarkar, S.; Sharan, M.; Abdulsalam, A.; Chudasama, R.; Dutta, D.; Jha, V.; Kumar, V.; Mohanty, A. K.; Pant, L. M.; Shukla, P.; Topkar, A.; Aziz, T.; Banerjee, S.; Bhowmik, S.; Chatterjee, R. M.; Dewanjee, R. K.; Dugad, S.; Ganguly, S.; Ghosh, S.; Guchait, M.; Gurtu, A.; Kole, G.; Kumar, S.; Mahakud, B.; Maity, M.; Majumder, G.; Mazumdar, K.; Mitra, S.; Mohanty, G. B.; Parida, B.; Sarkar, T.; Sudhakar, K.; Sur, N.; Sutar, B.; Wickramage, N.; Chauhan, S.; Dube, S.; Sharma, S.; Bakhshiansohi, H.; Behnamian, H.; Etesami, S. M.; Fahim, A.; Goldouzian, R.; Khakzad, M.; Mohammadi Najafabadi, M.; Naseri, M.; Paktinat Mehdiabadi, S.; Rezaei Hosseinabadi, F.; Safarzadeh, B.; Zeinali, M.; Felcini, M.; Grunewald, M.; Abbrescia, M.; Calabria, C.; Caputo, C.; Chhibra, S. S.; Colaleo, A.; Creanza, D.; Cristella, L.; de Filippis, N.; de Palma, M.; Fiore, L.; Iaselli, G.; Maggi, G.; Maggi, M.; Miniello, G.; My, S.; Nuzzo, S.; Pompili, A.; Pugliese, G.; Radogna, R.; Ranieri, A.; Selvaggi, G.; Silvestris, L.; Venditti, R.; Verwilligen, P.; Abbiendi, G.; Battilana, C.; Benvenuti, A. C.; Bonacorsi, D.; Braibant-Giacomelli, S.; Brigliadori, L.; Campanini, R.; Capiluppi, P.; Castro, A.; Cavallo, F. R.; Codispoti, G.; Cuffiani, M.; Dallavalle, G. M.; Fabbri, F.; Fanfani, A.; Fasanella, D.; Giacomelli, P.; Grandi, C.; Guiducci, L.; Marcellini, S.; Masetti, G.; Montanari, A.; Navarria, F. L.; Perrotta, A.; Rossi, A. M.; Rovelli, T.; Siroli, G. P.; Tosi, N.; Travaglini, R.; Cappello, G.; Chiorboli, M.; Costa, S.; Giordano, F.; Potenza, R.; Tricomi, A.; Tuve, C.; Barbagli, G.; Ciulli, V.; Civinini, C.; D'Alessandro, R.; Focardi, E.; Gonzi, S.; Gori, V.; Lenzi, P.; Meschini, M.; Paoletti, S.; Sguazzoni, G.; Tropiano, A.; Viliani, L.; Benussi, L.; Bianco, S.; Fabbri, F.; Piccolo, D.; Calvelli, V.; Ferro, F.; Lo Vetere, M.; Monge, M. R.; Robutti, E.; Tosi, S.; Brianza, L.; Dinardo, M. E.; Fiorendi, S.; Gennai, S.; Gerosa, R.; Ghezzi, A.; Govoni, P.; Malvezzi, S.; Manzoni, R. A.; Marzocchi, B.; Menasce, D.; Moroni, L.; Paganoni, M.; Pedrini, D.; Ragazzi, S.; Redaelli, N.; Tabarelli de Fatis, T.; Buontempo, S.; Cavallo, N.; di Guida, S.; Esposito, M.; Fabozzi, F.; Iorio, A. O. M.; Lanza, G.; Lista, L.; Meola, S.; Merola, M.; Paolucci, P.; Sciacca, C.; Thyssen, F.; Azzi, P.; Bacchetta, N.; Benato, L.; Bisello, D.; Boletti, A.; Branca, A.; Carlin, R.; Checchia, P.; Dall'Osso, M.; Dorigo, T.; Gasparini, F.; Gasparini, U.; Gozzelino, A.; Kanishchev, K.; Lacaprara, S.; Margoni, M.; Meneguzzo, A. T.; Montecassiano, F.; Passaseo, M.; Pazzini, J.; Pozzobon, N.; Ronchese, P.; Simonetto, F.; Torassa, E.; Tosi, M.; Zanetti, M.; Zotto, P.; Zucchetta, A.; Zumerle, G.; Braghieri, A.; Magnani, A.; Montagna, P.; Ratti, S. P.; Re, V.; Riccardi, C.; Salvini, P.; Vai, I.; Vitulo, P.; Alunni Solestizi, L.; Biasini, M.; Bilei, G. M.; Ciangottini, D.; Fanò, L.; Lariccia, P.; Mantovani, G.; Menichelli, M.; Saha, A.; Santocchia, A.; Spiezia, A.; Androsov, K.; Azzurri, P.; Bagliesi, G.; Bernardini, J.; Boccali, T.; Broccolo, G.; Castaldi, R.; Ciocci, M. A.; Dell'Orso, R.; Donato, S.; Fedi, G.; Foà, L.; Giassi, A.; Grippo, M. T.; Ligabue, F.; Lomtadze, T.; Martini, L.; Messineo, A.; Palla, F.; Rizzi, A.; Savoy-Navarro, A.; Serban, A. T.; Spagnolo, P.; Squillacioti, P.; Tenchini, R.; Tonelli, G.; Venturi, A.; Verdini, P. G.; Barone, L.; Cavallari, F.; D'Imperio, G.; Del Re, D.; Diemoz, M.; Gelli, S.; Jorda, C.; Longo, E.; Margaroli, F.; Meridiani, P.; Micheli, F.; Organtini, G.; Paramatti, R.; Preiato, F.; Rahatlou, S.; Rovelli, C.; Santanastasio, F.; Traczyk, P.; Amapane, N.; Arcidiacono, R.; Argiro, S.; Arneodo, M.; Bellan, R.; Biino, C.; Cartiglia, N.; Costa, M.; Covarelli, R.; de Remigis, P.; Degano, A.; Demaria, N.; Finco, L.; Mariotti, C.; Maselli, S.; Migliore, E.; Monaco, V.; Monteil, E.; Musich, M.; Obertino, M. M.; Pacher, L.; Pastrone, N.; Pelliccioni, M.; Pinna Angioni, G. L.; Ravera, F.; Romero, A.; Ruspa, M.; Sacchi, R.; Solano, A.; Staiano, A.; Tamponi, U.; Belforte, S.; Candelise, V.; Casarsa, M.; Cossutti, F.; Della Ricca, G.; Gobbo, B.; La Licata, C.; Marone, M.; Schizzi, A.; Umer, T.; Zanetti, A.; Chang, S.; Kropivnitskaya, A.; Nam, S. K.; Kim, D. H.; Kim, G. N.; Kim, M. S.; Kong, D. J.; Lee, S.; Oh, Y. D.; Sakharov, A.; Son, D. C.; Brochero Cifuentes, J. A.; Kim, H.; Kim, T. J.; Ryu, M. S.; Song, S.; Choi, S.; Go, Y.; Gyun, D.; Hong, B.; Jo, M.; Kim, H.; Kim, Y.; Lee, B.; Lee, K.; Lee, K. S.; Lee, S.; Park, S. K.; Roh, Y.; Yoo, H. D.; Choi, M.; Kim, H.; Kim, J. H.; Lee, J. S. H.; Park, I. C.; Ryu, G.; Choi, Y.; Choi, Y. K.; Goh, J.; Kim, D.; Kwon, E.; Lee, J.; Yu, I.; Juodagalvis, A.; Vaitkus, J.; Ahmed, I.; Ibrahim, Z. A.; Komaragiri, J. R.; Md Ali, M. A. B.; Mohamad Idris, F.; Wan Abdullah, W. A. T.; Yusli, M. 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V.; Vinogradov, A.; Baskakov, A.; Belyaev, A.; Boos, E.; Bunichev, V.; Dubinin, M.; Dudko, L.; Ershov, A.; Gribushin, A.; Klyukhin, V.; Kodolova, O.; Lokhtin, I.; Myagkov, I.; Obraztsov, S.; Perfilov, M.; Savrin, V.; Azhgirey, I.; Bayshev, I.; Bitioukov, S.; Kachanov, V.; Kalinin, A.; Konstantinov, D.; Krychkine, V.; Petrov, V.; Ryutin, R.; Sobol, A.; Tourtchanovitch, L.; Troshin, S.; Tyurin, N.; Uzunian, A.; Volkov, A.; Adzic, P.; Ekmedzic, M.; Milosevic, J.; Rekovic, V.; Alcaraz Maestre, J.; Calvo, E.; Cerrada, M.; Chamizo Llatas, M.; Colino, N.; de La Cruz, B.; Delgado Peris, A.; Domínguez Vázquez, D.; Escalante Del Valle, A.; Fernandez Bedoya, C.; Fernández Ramos, J. P.; Flix, J.; Fouz, M. C.; Garcia-Abia, P.; Gonzalez Lopez, O.; Goy Lopez, S.; Hernandez, J. M.; Josa, M. I.; Navarro de Martino, E.; Pérez-Calero Yzquierdo, A.; Puerta Pelayo, J.; Quintario Olmeda, A.; Redondo, I.; Romero, L.; Soares, M. S.; Albajar, C.; de Trocóniz, J. 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M.; Bloch, P.; Bocci, A.; Bonato, A.; Botta, C.; Breuker, H.; Camporesi, T.; Cerminara, G.; Colafranceschi, S.; D'Alfonso, M.; D'Enterria, D.; Dabrowski, A.; Daponte, V.; David, A.; de Gruttola, M.; de Guio, F.; de Roeck, A.; de Visscher, S.; di Marco, E.; Dobson, M.; Dordevic, M.; Du Pree, T.; Dupont, N.; Elliott-Peisert, A.; Franzoni, G.; Funk, W.; Gigi, D.; Gill, K.; Giordano, D.; Girone, M.; Glege, F.; Guida, R.; Gundacker, S.; Guthoff, M.; Hammer, J.; Hansen, M.; Harris, P.; Hegeman, J.; Innocente, V.; Janot, P.; Kirschenmann, H.; Kortelainen, M. J.; Kousouris, K.; Krajczar, K.; Lecoq, P.; Lourenço, C.; Lucchini, M. T.; Magini, N.; Malgeri, L.; Mannelli, M.; Martelli, A.; Masetti, L.; Meijers, F.; Mersi, S.; Meschi, E.; Moortgat, F.; Morovic, S.; Mulders, M.; Nemallapudi, M. V.; Neugebauer, H.; Orfanelli, S.; Orsini, L.; Pape, L.; Perez, E.; Petrilli, A.; Petrucciani, G.; Pfeiffer, A.; Piparo, D.; Racz, A.; Rolandi, G.; Rovere, M.; Ruan, M.; Sakulin, H.; Schäfer, C.; Schwick, C.; Sharma, A.; Silva, P.; Simon, M.; Sphicas, P.; Spiga, D.; Steggemann, J.; Stieger, B.; Stoye, M.; Takahashi, Y.; Treille, D.; Triossi, A.; Tsirou, A.; Veres, G. I.; Wardle, N.; Wöhri, H. K.; Zagozdzinska, A.; Zeuner, W. D.; Bertl, W.; Deiters, K.; Erdmann, W.; Horisberger, R.; Ingram, Q.; Kaestli, H. C.; Kotlinski, D.; Langenegger, U.; Renker, D.; Rohe, T.; Bachmair, F.; Bäni, L.; Bianchini, L.; Buchmann, M. A.; Casal, B.; Dissertori, G.; Dittmar, M.; Donegà, M.; Dünser, M.; Eller, P.; Grab, C.; Heidegger, C.; Hits, D.; Hoss, J.; Kasieczka, G.; Lustermann, W.; Mangano, B.; Marini, A. C.; Marionneau, M.; Martinez Ruiz Del Arbol, P.; Masciovecchio, M.; Meister, D.; Musella, P.; Nessi-Tedaldi, F.; Pandolfi, F.; Pata, J.; Pauss, F.; Perrozzi, L.; Peruzzi, M.; Quittnat, M.; Rossini, M.; Starodumov, A.; Takahashi, M.; Tavolaro, V. R.; Theofilatos, K.; Wallny, R.; Aarrestad, T. K.; Amsler, C.; Caminada, L.; Canelli, M. F.; Chiochia, V.; de Cosa, A.; Galloni, C.; Hinzmann, A.; Hreus, T.; Kilminster, B.; Lange, C.; Ngadiuba, J.; Pinna, D.; Robmann, P.; Ronga, F. J.; Salerno, D.; Yang, Y.; Cardaci, M.; Chen, K. H.; Doan, T. H.; Ferro, C.; Jain, Sh.; Khurana, R.; Konyushikhin, M.; Kuo, C. M.; Lin, W.; Lu, Y. J.; Volpe, R.; Yu, S. S.; Bartek, R.; Chang, P.; Chang, Y. H.; Chang, Y. W.; Chao, Y.; Chen, K. F.; Chen, P. H.; Dietz, C.; Fiori, F.; Grundler, U.; Hou, W.-S.; Hsiung, Y.; Liu, Y. F.; Lu, R.-S.; Miñano Moya, M.; Petrakou, E.; Tsai, J. F.; Tzeng, Y. M.; Asavapibhop, B.; Kovitanggoon, K.; Singh, G.; Srimanobhas, N.; Suwonjandee, N.; Adiguzel, A.; Bakirci, M. 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J.; Worm, S. D.; Baber, M.; Bainbridge, R.; Buchmuller, O.; Bundock, A.; Burton, D.; Casasso, S.; Citron, M.; Colling, D.; Corpe, L.; Cripps, N.; Dauncey, P.; Davies, G.; de Wit, A.; Della Negra, M.; Dunne, P.; Elwood, A.; Ferguson, W.; Fulcher, J.; Futyan, D.; Hall, G.; Iles, G.; Karapostoli, G.; Kenzie, M.; Lane, R.; Lucas, R.; Lyons, L.; Magnan, A.-M.; Malik, S.; Nash, J.; Nikitenko, A.; Pela, J.; Pesaresi, M.; Petridis, K.; Raymond, D. M.; Richards, A.; Rose, A.; Seez, C.; Tapper, A.; Uchida, K.; Vazquez Acosta, M.; Virdee, T.; Zenz, S. C.; Cole, J. E.; Hobson, P. R.; Khan, A.; Kyberd, P.; Leggat, D.; Leslie, D.; Reid, I. D.; Symonds, P.; Teodorescu, L.; Turner, M.; Borzou, A.; Call, K.; Dittmann, J.; Hatakeyama, K.; Kasmi, A.; Liu, H.; Pastika, N.; Charaf, O.; Cooper, S. 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R.; Luthra, A.; Malberti, M.; Olmedo Negrete, M.; Shrinivas, A.; Wei, H.; Wimpenny, S.; Branson, J. G.; Cerati, G. B.; Cittolin, S.; D'Agnolo, R. T.; Holzner, A.; Kelley, R.; Klein, D.; Letts, J.; MacNeill, I.; Olivito, D.; Padhi, S.; Pieri, M.; Sani, M.; Sharma, V.; Simon, S.; Tadel, M.; Vartak, A.; Wasserbaech, S.; Welke, C.; Würthwein, F.; Yagil, A.; Zevi Della Porta, G.; Barge, D.; Bradmiller-Feld, J.; Campagnari, C.; Dishaw, A.; Dutta, V.; Flowers, K.; Franco Sevilla, M.; Geffert, P.; George, C.; Golf, F.; Gouskos, L.; Gran, J.; Incandela, J.; Justus, C.; McColl, N.; Mullin, S. D.; Richman, J.; Stuart, D.; Suarez, I.; To, W.; West, C.; Yoo, J.; Anderson, D.; Apresyan, A.; Bornheim, A.; Bunn, J.; Chen, Y.; Duarte, J.; Mott, A.; Newman, H. B.; Pena, C.; Pierini, M.; Spiropulu, M.; Vlimant, J. R.; Xie, S.; Zhu, R. Y.; Azzolini, V.; Calamba, A.; Carlson, B.; Ferguson, T.; Iiyama, Y.; Paulini, M.; Russ, J.; Sun, M.; Vogel, H.; Vorobiev, I.; Cumalat, J. P.; Ford, W. T.; Gaz, A.; Jensen, F.; Johnson, A.; Krohn, M.; Mulholland, T.; Nauenberg, U.; Smith, J. G.; Stenson, K.; Wagner, S. R.; Alexander, J.; Chatterjee, A.; Chaves, J.; Chu, J.; Dittmer, S.; Eggert, N.; Mirman, N.; Nicolas Kaufman, G.; Patterson, J. R.; Rinkevicius, A.; Ryd, A.; Skinnari, L.; Soffi, L.; Sun, W.; Tan, S. M.; Teo, W. D.; Thom, J.; Thompson, J.; Tucker, J.; Weng, Y.; Wittich, P.; Abdullin, S.; Albrow, M.; Anderson, J.; Apollinari, G.; Bauerdick, L. A. T.; Beretvas, A.; Berryhill, J.; Bhat, P. C.; Bolla, G.; Burkett, K.; Butler, J. N.; Cheung, H. W. K.; Chlebana, F.; Cihangir, S.; Elvira, V. D.; Fisk, I.; Freeman, J.; Gottschalk, E.; Gray, L.; Green, D.; Grünendahl, S.; Gutsche, O.; Hanlon, J.; Hare, D.; Harris, R. M.; Hirschauer, J.; Hooberman, B.; Hu, Z.; Jindariani, S.; Johnson, M.; Joshi, U.; Jung, A. W.; Klima, B.; Kreis, B.; Kwan, S.; Lammel, S.; Linacre, J.; Lincoln, D.; Lipton, R.; Liu, T.; Lopes de Sá, R.; Lykken, J.; Maeshima, K.; Marraffino, J. M.; Martinez Outschoorn, V. I.; Maruyama, S.; Mason, D.; McBride, P.; Merkel, P.; Mishra, K.; Mrenna, S.; Nahn, S.; Newman-Holmes, C.; O'Dell, V.; Pedro, K.; Prokofyev, O.; Rakness, G.; Sexton-Kennedy, E.; Soha, A.; Spalding, W. J.; Spiegel, L.; Taylor, L.; Tkaczyk, S.; Tran, N. V.; Uplegger, L.; Vaandering, E. W.; Vernieri, C.; Verzocchi, M.; Vidal, R.; Weber, H. A.; Whitbeck, A.; Yang, F.; Yin, H.; Acosta, D.; Avery, P.; Bortignon, P.; Bourilkov, D.; Carnes, A.; Carver, M.; Curry, D.; Das, S.; di Giovanni, G. P.; Field, R. D.; Fisher, M.; Furic, I. K.; Hugon, J.; Konigsberg, J.; Korytov, A.; Low, J. F.; Ma, P.; Matchev, K.; Mei, H.; Milenovic, P.; Mitselmakher, G.; Muniz, L.; Rank, D.; Rossin, R.; Shchutska, L.; Snowball, M.; Sperka, D.; Wang, J.; Wang, S.; Yelton, J.; Hewamanage, S.; Linn, S.; Markowitz, P.; Martinez, G.; Rodriguez, J. L.; Ackert, A.; Adams, J. R.; Adams, T.; Askew, A.; Bochenek, J.; Diamond, B.; Haas, J.; Hagopian, S.; Hagopian, V.; Johnson, K. F.; Khatiwada, A.; Prosper, H.; Veeraraghavan, V.; Weinberg, M.; Bhopatkar, V.; Hohlmann, M.; Kalakhety, H.; Mareskas-Palcek, D.; Roy, T.; Yumiceva, F.; Adams, M. R.; Apanasevich, L.; Berry, D.; Betts, R. R.; Bucinskaite, I.; Cavanaugh, R.; Evdokimov, O.; Gauthier, L.; Gerber, C. E.; Hofman, D. J.; Kurt, P.; O'Brien, C.; Sandoval Gonzalez, I. D.; Silkworth, C.; Turner, P.; Varelas, N.; Wu, Z.; Zakaria, M.; Bilki, B.; Clarida, W.; Dilsiz, K.; Durgut, S.; Gandrajula, R. P.; Haytmyradov, M.; Khristenko, V.; Merlo, J.-P.; Mermerkaya, H.; Mestvirishvili, A.; Moeller, A.; Nachtman, J.; Ogul, H.; Onel, Y.; Ozok, F.; Penzo, A.; Snyder, C.; Tan, P.; Tiras, E.; Wetzel, J.; Yi, K.; Anderson, I.; Barnett, B. A.; Blumenfeld, B.; Fehling, D.; Feng, L.; Gritsan, A. V.; Maksimovic, P.; Martin, C.; Nash, K.; Osherson, M.; Swartz, M.; Xiao, M.; Xin, Y.; Baringer, P.; Bean, A.; Benelli, G.; Bruner, C.; Gray, J.; Kenny, R. P., III; Majumder, D.; Malek, M.; Murray, M.; Noonan, D.; Sanders, S.; Stringer, R.; Wang, Q.; Wood, J. S.; Chakaberia, I.; Ivanov, A.; Kaadze, K.; Khalil, S.; Makouski, M.; Maravin, Y.; Mohammadi, A.; Saini, L. K.; Skhirtladze, N.; Svintradze, I.; Toda, S.; Lange, D.; Rebassoo, F.; Wright, D.; Anelli, C.; Baden, A.; Baron, O.; Belloni, A.; Calvert, B.; Eno, S. C.; Ferraioli, C.; Gomez, J. A.; Hadley, N. J.; Jabeen, S.; Kellogg, R. G.; Kolberg, T.; Kunkle, J.; Lu, Y.; Mignerey, A. C.; Shin, Y. H.; Skuja, A.; Tonjes, M. B.; Tonwar, S. C.; Apyan, A.; Barbieri, R.; Baty, A.; Bierwagen, K.; Brandt, S.; Busza, W.; Cali, I. A.; Demiragli, Z.; Di Matteo, L.; Gomez Ceballos, G.; Goncharov, M.; Gulhan, D.; Innocenti, G. M.; Klute, M.; Kovalskyi, D.; Lai, Y. S.; Lee, Y.-J.; Levin, A.; Luckey, P. D.; McGinn, C.; Mironov, C.; Niu, X.; Paus, C.; Ralph, D.; Roland, C.; Roland, G.; Salfeld-Nebgen, J.; Stephans, G. S. F.; Sumorok, K.; Varma, M.; Velicanu, D.; Veverka, J.; Wang, J.; Wang, T. W.; Wyslouch, B.; Yang, M.; Zhukova, V.; Dahmes, B.; Finkel, A.; Gude, A.; Hansen, P.; Kalafut, S.; Kao, S. C.; Klapoetke, K.; Kubota, Y.; Lesko, Z.; Mans, J.; Nourbakhsh, S.; Ruckstuhl, N.; Rusack, R.; Tambe, N.; Turkewitz, J.; Acosta, J. G.; Oliveros, S.; Avdeeva, E.; Bloom, K.; Bose, S.; Claes, D. R.; Dominguez, A.; Fangmeier, C.; Gonzalez Suarez, R.; Kamalieddin, R.; Keller, J.; Knowlton, D.; Kravchenko, I.; Lazo-Flores, J.; Meier, F.; Monroy, J.; Ratnikov, F.; Siado, J. E.; Snow, G. R.; Alyari, M.; Dolen, J.; George, J.; Godshalk, A.; Iashvili, I.; Kaisen, J.; Kharchilava, A.; Kumar, A.; Rappoccio, S.; Alverson, G.; Barberis, E.; Baumgartel, D.; Chasco, M.; Hortiangtham, A.; Massironi, A.; Morse, D. M.; Nash, D.; Orimoto, T.; Teixeira de Lima, R.; Trocino, D.; Wang, R.-J.; Wood, D.; Zhang, J.; Hahn, K. A.; Kubik, A.; Mucia, N.; Odell, N.; Pollack, B.; Pozdnyakov, A.; Schmitt, M.; Stoynev, S.; Sung, K.; Trovato, M.; Velasco, M.; Won, S.; Brinkerhoff, A.; Dev, N.; Hildreth, M.; Jessop, C.; Karmgard, D. J.; Kellams, N.; Lannon, K.; Lynch, S.; Marinelli, N.; Meng, F.; Mueller, C.; Musienko, Y.; Pearson, T.; Planer, M.; Reinsvold, A.; Ruchti, R.; Smith, G.; Taroni, S.; Valls, N.; Wayne, M.; Wolf, M.; Woodard, A.; Antonelli, L.; Brinson, J.; Bylsma, B.; Durkin, L. S.; Flowers, S.; Hart, A.; Hill, C.; Hughes, R.; Kotov, K.; Ling, T. Y.; Liu, B.; Luo, W.; Puigh, D.; Rodenburg, M.; Winer, B. L.; Wulsin, H. W.; Driga, O.; Elmer, P.; Hardenbrook, J.; Hebda, P.; Koay, S. A.; Lujan, P.; Marlow, D.; Medvedeva, T.; Mooney, M.; Olsen, J.; Palmer, C.; Piroué, P.; Quan, X.; Saka, H.; Stickland, D.; Tully, C.; Werner, J. S.; Zuranski, A.; Malik, S.; Barnes, V. E.; Benedetti, D.; Bortoletto, D.; Gutay, L.; Jha, M. K.; Jones, M.; Jung, K.; Kress, M.; Miller, D. H.; Neumeister, N.; Primavera, F.; Radburn-Smith, B. C.; Shi, X.; Shipsey, I.; Silvers, D.; Sun, J.; Svyatkovskiy, A.; Wang, F.; Xie, W.; Xu, L.; Zablocki, J.; Parashar, N.; Stupak, J.; Adair, A.; Akgun, B.; Chen, Z.; Ecklund, K. M.; Geurts, F. J. M.; Guilbaud, M.; Li, W.; Michlin, B.; Northup, M.; Padley, B. P.; Redjimi, R.; Roberts, J.; Rorie, J.; Tu, Z.; Zabel, J.; Betchart, B.; Bodek, A.; de Barbaro, P.; Demina, R.; Eshaq, Y.; Ferbel, T.; Galanti, M.; Garcia-Bellido, A.; Goldenzweig, P.; Han, J.; Harel, A.; Hindrichs, O.; Khukhunaishvili, A.; Petrillo, G.; Verzetti, M.; Demortier, L.; Arora, S.; Barker, A.; Chou, J. P.; Contreras-Campana, C.; Contreras-Campana, E.; Duggan, D.; Ferencek, D.; Gershtein, Y.; Gray, R.; Halkiadakis, E.; Hidas, D.; Hughes, E.; Kaplan, S.; Kunnawalkam Elayavalli, R.; Lath, A.; Panwalkar, S.; Park, M.; Salur, S.; Schnetzer, S.; Sheffield, D.; Somalwar, S.; Stone, R.; Thomas, S.; Thomassen, P.; Walker, M.; Foerster, M.; Riley, G.; Rose, K.; Spanier, S.; York, A.; Bouhali, O.; Castaneda Hernandez, A.; Dalchenko, M.; de Mattia, M.; Delgado, A.; Dildick, S.; Eusebi, R.; Flanagan, W.; Gilmore, J.; Kamon, T.; Krutelyov, V.; Montalvo, R.; Mueller, R.; Osipenkov, I.; Pakhotin, Y.; Patel, R.; Perloff, A.; Roe, J.; Rose, A.; Safonov, A.; Tatarinov, A.; Ulmer, K. A.; Akchurin, N.; Cowden, C.; Damgov, J.; Dragoiu, C.; Dudero, P. R.; Faulkner, J.; Kunori, S.; Lamichhane, K.; Lee, S. W.; Libeiro, T.; Undleeb, S.; Volobouev, I.; Appelt, E.; Delannoy, A. G.; Greene, S.; Gurrola, A.; Janjam, R.; Johns, W.; Maguire, C.; Mao, Y.; Melo, A.; Sheldon, P.; Snook, B.; Tuo, S.; Velkovska, J.; Xu, Q.; Arenton, M. W.; Boutle, S.; Cox, B.; Francis, B.; Goodell, J.; Hirosky, R.; Ledovskoy, A.; Li, H.; Lin, C.; Neu, C.; Wolfe, E.; Wood, J.; Xia, F.; Clarke, C.; Harr, R.; Karchin, P. E.; Kottachchi Kankanamge Don, C.; Lamichhane, P.; Sturdy, J.; Belknap, D. A.; Carlsmith, D.; Cepeda, M.; Christian, A.; Dasu, S.; Dodd, L.; Duric, S.; Friis, E.; Gomber, B.; Hall-Wilton, R.; Herndon, M.; Hervé, A.; Klabbers, P.; Lanaro, A.; Levine, A.; Long, K.; Loveless, R.; Mohapatra, A.; Ojalvo, I.; Perry, T.; Pierro, G. A.; Polese, G.; Ross, I.; Ruggles, T.; Sarangi, T.; Savin, A.; Sharma, A.; Smith, N.; Smith, W. H.; Taylor, D.; Woods, N.

    2016-04-01

    The first search for a heavy charged vector boson in the final state with a tau lepton and a neutrino is reported, using 19.7 fb-1 of LHC data at √{ s} = 8 TeV. A signal would appear as an excess of events with high transverse mass, where the standard model background is low. No excess is observed. Limits are set on a model in which the W‧ decays preferentially to fermions of the third generation. These results substantially extend previous constraints on this model. Masses below 2.0 to 2.7 TeV are excluded, depending on the model parameters. In addition, the existence of a W‧ boson with universal fermion couplings is excluded at 95% confidence level, for W‧ masses below 2.7 TeV. For further reinterpretation a model-independent limit on potential signals for various transverse mass thresholds is also presented.

  2. Search for W' decaying to tau lepton and neutrino in proton-proton collisions at $\\sqrt{s}$ = 8 TeV

    SciTech Connect

    Khachatryan, Vardan

    2015-08-19

    We found that the first search for a heavy charged vector boson in the final state with a tau lepton and a neutrino is reported, using 19.7 fb-1 of LHC data at √s = 8 TeV. A signal would appear as an excess of events in kinematic regions where the standard model background is low. No excess is observed. Limits are set on a model in which the W' decays preferentially to fermions of the third generation. Our results substantially extend previous constraints on this model. Masses below 2.0 to 2.7 TeV are excluded, depending on the model parameters. In addition, the existence of a W' boson with universal fermion couplings is excluded at 95% confidence level, for W' masses below 2.7 TeV.

  3. Estimate of the branching fraction {tau}{sup -}{yields}{eta}{pi}{sup -}{nu}{sub {tau}}, the a{sub 0}{sup -}(980), and nonstandard weak interactions

    SciTech Connect

    Nussinov, S.; Soffer, A.

    2008-08-01

    We consider the 'second-class current' decay {tau}{sup -}{yields}{pi}{sup -}{eta}{nu}{sub {tau}} from several points of view. We first focus on the decay rate as expected within standard weak interaction and QCD due to isospin violation. The decay contributions divide into P- and S-wave parts. The former can be reliably estimated using the {rho}{eta}{pi} coupling inferred from the rates and Dalitz-plot distributions of {eta}{yields}3{pi} decays. The somewhat larger S-wave part, which was previously computed using chiral perturbation theory, is estimated from a simple qq model. Both estimates of the S-wave part depend on whether the a{sub 0}(980) scalar particle is a qq or some other (4-quark) state. Finally, we discuss genuinely new, non-V-A scalar weak interactions. The {tau}{sup -}{yields}{pi}{sup -}{eta}{nu}{sub {tau}} decay provides information on this question, which nicely complements that from precision {beta} decay experiments. In summary, we discuss the possible implications of putative values of the branching fraction B({tau}{sup -}{yields}{pi}{sup -}{eta}{nu}{sub {tau}}). In the case of larger values, in particular, of the S-wave part, not only will detection of the decay be more likely and more reliable, its implications will be more far-reaching and interesting.

  4. Amplification of Tau Fibrils from Minute Quantities of Seeds

    PubMed Central

    2014-01-01

    The propagation of Tau pathology in Alzheimers disease (AD) is thought to proceed through templated conversion of Tau protein into fibrils and cell-to-cell transfer of elongation-competent seeds. To investigate the efficiency of Tau conversion, we adapted the protein misfolding cyclic amplification assay used for the conversion of prions. Utilizing heparin as a cofactor and employing repetitive cycles of shearing and growth, synthetic Tau fibrils and Tau fibrils in AD brain extract are progressively amplified. Concurrently, self-nucleation is suppressed. The results highlight breakage-induced replication of Tau fibrils as a potential facilitator of disease spread. PMID:25153692

  5. Search for astrophysical tau neutrinos in three years of IceCube data

    NASA Astrophysics Data System (ADS)

    Aartsen, M. G.; Abraham, K.; Ackermann, M.; Adams, J.; Aguilar, J. A.; Ahlers, M.; Ahrens, M.; Altmann, D.; Anderson, T.; Ansseau, I.; Archinger, M.; Arguelles, C.; Arlen, T. C.; Auffenberg, J.; Bai, X.; Barwick, S. W.; Baum, V.; Bay, R.; Beatty, J. J.; Becker Tjus, J.; Becker, K.-H.; Beiser, E.; BenZvi, S.; Berghaus, P.; Berley, D.; Bernardini, E.; Bernhard, A.; Besson, D. Z.; Binder, G.; Bindig, D.; Bissok, M.; Blaufuss, E.; Blumenthal, J.; Boersma, D. J.; Bohm, C.; Börner, M.; Bos, F.; Bose, D.; Böser, S.; Botner, O.; Braun, J.; Brayeur, L.; Bretz, H.-P.; Buzinsky, N.; Casey, J.; Casier, M.; Cheung, E.; Chirkin, D.; Christov, A.; Clark, K.; Classen, L.; Coenders, S.; Cowen, D. F.; Cruz Silva, A. H.; Daughhetee, J.; Davis, J. C.; Day, M.; de André, J. P. A. M.; De Clercq, C.; del Pino Rosendo, E.; Dembinski, H.; De Ridder, S.; Desiati, P.; de Vries, K. D.; de Wasseige, G.; de With, M.; DeYoung, T.; Díaz-Vélez, J. C.; di Lorenzo, V.; Dumm, J. P.; Dunkman, M.; Eagan, R.; Eberhardt, B.; Ehrhardt, T.; Eichmann, B.; Euler, S.; Evenson, P. A.; Fadiran, O.; Fahey, S.; Fazely, A. R.; Fedynitch, A.; Feintzeig, J.; Felde, J.; Filimonov, K.; Finley, C.; Fischer-Wasels, T.; Flis, S.; Fösig, C.-C.; Fuchs, T.; Gaisser, T. K.; Gaior, R.; Gallagher, J.; Gerhardt, L.; Ghorbani, K.; Gier, D.; Gladstone, L.; Glagla, M.; Glüsenkamp, T.; Goldschmidt, A.; Golup, G.; Gonzalez, J. G.; Góra, D.; Grant, D.; Groh, J. C.; Groß, A.; Ha, C.; Haack, C.; Haj Ismail, A.; Hallgren, A.; Halzen, F.; Hansen, E.; Hansmann, B.; Hanson, K.; Hebecker, D.; Heereman, D.; Helbing, K.; Hellauer, R.; Hickford, S.; Hignight, J.; Hill, G. C.; Hoffman, K. D.; Hoffmann, R.; Holzapfel, K.; Homeier, A.; Hoshina, K.; Huang, F.; Huber, M.; Huelsnitz, W.; Hulth, P. O.; Hultqvist, K.; In, S.; Ishihara, A.; Jacobi, E.; Japaridze, G. S.; Jero, K.; Jurkovic, M.; Kappes, A.; Karg, T.; Karle, A.; Kauer, M.; Keivani, A.; Kelley, J. L.; Kemp, J.; Kheirandish, A.; Kiryluk, J.; Kläs, J.; Klein, S. R.; Kohnen, G.; Koirala, R.; Kolanoski, H.; Konietz, R.; Köpke, L.; Kopper, C.; Kopper, S.; Koskinen, D. J.; Kowalski, M.; Krings, K.; Kroll, G.; Kroll, M.; Kunnen, J.; Kurahashi, N.; Kuwabara, T.; Labare, M.; Lanfranchi, J. L.; Larson, M. J.; Lesiak-Bzdak, M.; Leuermann, M.; Leuner, J.; Lu, L.; Lünemann, J.; Madsen, J.; Maggi, G.; Mahn, K. B. M.; Maruyama, R.; Mase, K.; Matis, H. S.; Maunu, R.; McNally, F.; Meagher, K.; Medici, M.; Meli, A.; Menne, T.; Merino, G.; Meures, T.; Miarecki, S.; Middell, E.; Middlemas, E.; Mohrmann, L.; Montaruli, T.; Morse, R.; Nahnhauer, R.; Naumann, U.; Neer, G.; Niederhausen, H.; Nowicki, S. C.; Nygren, D. R.; Obertacke, A.; Olivas, A.; Omairat, A.; O'Murchadha, A.; Palczewski, T.; Pandya, H.; Pankova, D. V.; Paul, L.; Pepper, J. A.; Pérez de los Heros, C.; Pfendner, C.; Pieloth, D.; Pinat, E.; Posselt, J.; Price, P. B.; Przybylski, G. T.; Pütz, J.; Quinnan, M.; Raab, C.; Rädel, L.; Rameez, M.; Rawlins, K.; Reimann, R.; Relich, M.; Resconi, E.; Rhode, W.; Richman, M.; Richter, S.; Riedel, B.; Robertson, S.; Rongen, M.; Rott, C.; Ruhe, T.; Ryckbosch, D.; Saba, S. M.; Sabbatini, L.; Sander, H.-G.; Sandrock, A.; Sandroos, J.; Sarkar, S.; Schatto, K.; Scheriau, F.; Schimp, M.; Schmidt, T.; Schmitz, M.; Schoenen, S.; Schöneberg, S.; Schönwald, A.; Schulte, L.; Seckel, D.; Seunarine, S.; Smith, M. W. E.; Soldin, D.; Song, M.; Spiczak, G. M.; Spiering, C.; Stahlberg, M.; Stamatikos, M.; Stanev, T.; Stanisha, N. A.; Stasik, A.; Stezelberger, T.; Stokstad, R. G.; Stößl, A.; Ström, R.; Strotjohann, N. L.; Sullivan, G. W.; Sutherland, M.; Taavola, H.; Taboada, I.; Tatar, J.; Ter-Antonyan, S.; Terliuk, A.; Tešić, G.; Tilav, S.; Toale, P. A.; Tobin, M. N.; Toscano, S.; Tosi, D.; Tselengidou, M.; Turcati, A.; Unger, E.; Usner, M.; Vallecorsa, S.; Vandenbroucke, J.; van Eijndhoven, N.; Vanheule, S.; van Santen, J.; Veenkamp, J.; Vehring, M.; Voge, M.; Vraeghe, M.; Walck, C.; Wallace, A.; Wallraff, M.; Wandkowsky, N.; Weaver, Ch.; Wendt, C.; Westerhoff, S.; Whelan, B. J.; Whitehorn, N.; Wiebe, K.; Wiebusch, C. H.; Wille, L.; Williams, D. R.; Wissing, H.; Wolf, M.; Wood, T. R.; Woschnagg, K.; Xu, D. L.; Xu, X. W.; Xu, Y.; Yanez, J. P.; Yodh, G.; Yoshida, S.; Zoll, M.; IceCube Collaboration

    2016-01-01

    The IceCube Neutrino Observatory has observed a diffuse flux of TeV-PeV astrophysical neutrinos at 5.7 σ significance from an all-flavor search. The direct detection of tau neutrinos in this flux has yet to occur. Tau neutrinos become distinguishable from other flavors in IceCube at energies above a few hundred TeV, when the cascade from the tau neutrino charged current interaction becomes resolvable from the cascade from the tau lepton decay. This paper presents results from the first dedicated search for tau neutrinos with energies between 214 TeV and 72 PeV in the full IceCube detector. The analysis searches for IceCube optical sensors that observe two separate pulses in a single event—one from the tau neutrino interaction and a second from the tau decay. No candidate events were observed in three years of IceCube data. For the first time, a differential upper limit on astrophysical tau neutrinos is derived around the PeV energy region, which is nearly 3 orders of magnitude lower in energy than previous limits from dedicated tau neutrino searches.

  6. PICALM modulates autophagy activity and tau accumulation

    PubMed Central

    Moreau, Kevin; Fleming, Angeleen; Imarisio, Sara; Lopez Ramirez, Ana; Mercer, Jacob L.; Jimenez-Sanchez, Maria; Bento, Carla F.; Puri, Claudia; Zavodszky, Eszter; Siddiqi, Farah; Lavau, Catherine P.; Betton, Maureen; O’Kane, Cahir J.; Wechsler, Daniel S.; Rubinsztein, David C.

    2014-01-01

    Genome-wide association studies have identified several loci associated with Alzheimer’s disease (AD), including proteins involved in endocytic trafficking such as PICALM/CALM (phosphatidylinositol binding clathrin assembly protein). It is unclear how these loci may contribute to AD pathology. Here we show that CALM modulates autophagy and alters clearance of tau, a protein which is a known autophagy substrate and which is causatively linked to AD, both in vitro and in vivo. Furthermore, altered CALM expression exacerbates tau-mediated toxicity in zebrafish transgenic models. CALM influences autophagy by regulating the endocytosis of SNAREs, such as VAMP2, VAMP3 and VAMP8, which have diverse effects on different stages of the autophagy pathway, from autophagosome formation to autophagosome degradation. This study suggests that the AD genetic risk factor CALM modulates autophagy, and this may affect disease in a number of ways including modulation of tau turnover. PMID:25241929

  7. Pathological tau disrupts ongoing network activity.

    PubMed

    Menkes-Caspi, Noa; Yamin, Hagar G; Kellner, Vered; Spires-Jones, Tara L; Cohen, Dana; Stern, Edward A

    2015-03-01

    Pathological tau leads to dementia and neurodegeneration in tauopathies, including Alzheimer's disease. It has been shown to disrupt cellular and synaptic functions, yet its effects on the function of the intact neocortical network remain unknown. Using in vivo intracellular and extracellular recordings, we measured ongoing activity of neocortical pyramidal cells during various arousal states in the rTg4510 mouse model of tauopathy, prior to significant cell death, when only a fraction of the neurons show pathological tau. In transgenic mice, membrane potential oscillations are slower during slow-wave sleep and under anesthesia. Intracellular recordings revealed that these changes are due to longer Down states and state transitions of membrane potentials. Firing rates of transgenic neurons are reduced, and firing patterns within Up states are altered, with longer latencies and inter-spike intervals. By changing the activity patterns of a subpopulation of affected neurons, pathological tau reduces the activity of the neocortical network. PMID:25704951

  8. Inhibition of tau fibrillization by oleocanthal via reaction with the amino groups of tau

    PubMed Central

    Li, Wenkai; Sperry, Jeffrey B.; Crowe, Alex; Trojanowski, John Q.; Smith, Amos B.; Lee, Virginia M.-Y.

    2009-01-01

    Tau is a microtubule-associated protein that promotes microtubule assembly and stability. In Alzheimer's disease and related tauopathies, tau fibrillizes and aggregates into neurofibrillary tangles. Recently, oleocanthal isolated from extra virgin olive oil was found to display non-steroidal anti-inflammatory activity similar to ibuprofen. Since our unpublished data indicates an inhibitory effect of oleocanthal on Aβ fibrillization, we reasoned that it might inhibit tau fibrillization as well. Herein we demonstrate that oleocanthal abrogates fibrillization of tau by locking tau into the naturally unfolded state. Using PHF6 consisting of the amino acid residues VQIVYK, a hexapeptide within the third repeat of tau that is essential for fibrillization, we show that oleocanthal forms an adduct with the lysine via initial Schiff base formation. Structure and function studies demonstrate that the two aldehyde groups of oleocanthal are required for the inhibitory activity. These two aldehyde groups show certain specificity when titrated with free lysine and oleocanthal does not significantly affect the normal function of tau. These findings provide a potential scheme for the development of novel therapies for neurodegenerative tauopathies. PMID:19549281

  9. Structural Determinants of Tau Aggregation Inhibitor Potency*

    PubMed Central

    Schafer, Kelsey N.; Cisek, Katryna; Huseby, Carol J.; Chang, Edward; Kuret, Jeff

    2013-01-01

    Small-molecule Tau aggregation inhibitors are under investigation as potential therapeutic agents against Alzheimer disease. Many such inhibitors have been identified in vitro, but their potency-driving features, and their molecular targets in the Tau aggregation pathway, have resisted identification. Previously we proposed ligand polarizability, a measure of electron delocalization, as a candidate descriptor of inhibitor potency. Here we tested this hypothesis by correlating the ground state polarizabilities of cyanine, phenothiazine, and arylmethine derivatives calculated using ab initio quantum methods with inhibitory potency values determined in the presence of octadecyl sulfate inducer under reducing conditions. A series of rhodanine analogs was analyzed as well using potency values disclosed in the literature. Results showed that polarizability and inhibitory potency directly correlated within all four series. To identify putative binding targets, representative members of the four chemotypes were added to aggregation reactions, where they were found to stabilize soluble, but SDS-resistant Tau species at the expense of filamentous aggregates. Using SDS resistance as a secondary assay, and a library of Tau deletion and missense mutants as targets, interaction with cyanine was localized to the microtubule binding repeat region. Moreover, the SDS-resistant phenotype was completely dependent on the presence of octadecyl sulfate inducer, but not intact PHF6/PH6* hexapeptide motifs, indicating that cyanine interacted with a species in the aggregation pathway prior to nucleus formation. Together the data suggest that flat, highly polarizable ligands inhibit Tau aggregation by interacting with folded species in the aggregation pathway and driving their assembly into soluble but highly stable Tau oligomers. PMID:24072703

  10. Tau phosphorylation and tau mislocalization mediate soluble A? oligomer-induced AMPA glutamate receptor signaling deficits

    PubMed Central

    Miller, Eric C.; Teravskis, Peter J.; Dummer, Benjamin W.; Zhao, Xiaohui; Huganir, Richard L.; Liao, Dezhi

    2014-01-01

    In our previous studies, phosphorylation-dependent tau mislocalization to dendritic spines resulted in early cognitive and synaptic deficits. It is well known that amyloid beta (A?) oligomers cause synaptic dysfunction by inducing calcineurin-dependent AMPA receptor (AMPAR) internalization. However, it is unknown whether A?-induced synaptic deficits depend upon tau phosphorylation. It is also unknown whether changes in tau can cause calcineurin-dependent loss of AMPARs in synapses. Here, we show that tau mislocalizes to dendritic spines in cultured hippocampal neurons from APPSwe Alzheimers disease (AD)-transgenenic mice and in cultured rat hippocampal neurons treated with soluble A? oligomers. Interestingly, A? treatment also impairs synaptic function by decreasing the amplitude of miniature excitatory postsynaptic currents (mEPSCs). The above tau mislocalization and A?-induced synaptic impairment are both diminished by the expression of AP tau, indicating that these events require tau phosphorylation. The phosphatase activity of calcineurin is important for AMPAR internalization via dephosphorylation of GluA1 residue S845. The effects of A? oligomers on mEPSCs are blocked by the calcineurin inhibitor FK506. A?-induced loss of AMPARs is diminished in neurons from knock-in mice expressing S845A mutant GluA1 AMPA glutamate receptor subunits. This finding suggests that changes in phosphorylation state at S845 are involved in this pathogenic cascade. Furthermore, FK506 rescues deficits in surface AMPAR clustering on dendritic spines in neurons cultured from transgenic mice expressing P301L tau proteins. Together, our results support the role of tau and calcineurin as two intermediate signaling molecules between A? initiation and eventual synaptic dysfunction early in AD pathogenesis. PMID:24713000

  11. Cell-based Models To Investigate Tau Aggregation

    PubMed Central

    Lim, Sungsu; Haque, Md. Mamunul; Kim, Dohee; Kim, Dong Jin; Kim, Yun Kyung

    2014-01-01

    Accumulation of abnormal tau aggregates in neuron is an important pathological signature in multiple neurodegenerative disorders including Alzheimer's disease. Tau is a neuron specific microtubule-associated protein that regulates microtubule stability, which is critical for axonal outgrowth and synaptic plasticity. In a pathological condition, tau dissociates from microtubules and forms insoluble aggregates called neurofibrillary tangles (NFTs). The accumulation of NFTs in neuron directly correlates with microtubule dysfunction and neuronal degeneration. Due to the pathophysiological importance of tau, great efforts have been made to understand tau aggregation processes and find therapeutics to halt or reverse the processes. However, progress has been slow due to the lack of a suitable method for monitoring tau aggregation. In this mini-review, we will review the conventional methods for studying tau aggregation, and introduce recent cell-based sensor approaches that allow monitoring tau aggregation in living cells. PMID:25505502

  12. Atmospheric tau neutrinos in a multikiloton liquid argon detector

    SciTech Connect

    Conrad, Janet; Gouvea, Andre de; Shalgar, Shashank; Spitz, Joshua

    2010-11-01

    An ultralarge liquid argon time projection chamber based neutrino detector will have the uncommon ability to detect atmospheric {nu}{sub {tau}}/{nu}{tau} events. This paper discusses the most promising modes for identifying charged current {nu}{sub {tau}}/{nu}{tau}, and shows that, with simple kinematic cuts, {approx}30 {nu}{sub {tau}}+{nu}{tau} interactions can be isolated in a 100 kt{center_dot}yr exposure, with greater than 4{sigma} significance. This sample is sufficient to perform flux-averaged total cross-section and cross-section shape parametrization measurements--the first steps toward using {nu}{sub {tau}}/{nu}{tau} to search for physics beyond the standard model.

  13. Tau neurotoxicity and rescue in animal models of human Tauopathies.

    PubMed

    Krüger, Lars; Mandelkow, Eva Maria

    2016-02-01

    Pathological Tau is a hallmark of various neuronal disorders and spreads in the brain of Alzheimer patients in a well-defined manner. Beside Tau's main function in stabilizing microtubules for axonal transport, a variety of novel functions for neurons and glia have emerged recently. Tau regulates the susceptibility to hyperexcitation and plays a role in neuron-glia contact formation. Studies implicate soluble oligomeric species of Tau, rather than insoluble aggregates, as more detrimental to proper neuronal function. Tau is not exclusively intracellular; instead Tau can be released into the extracellular space. This has led to the hypothesis of a prion-disease like mechanism to explain the stereotypical progression of Tau. Targeting pathological Tau with antibodies or aggregation inhibitors may help to prevent pathology. PMID:26431808

  14. A precision measurement of the Z{sup 0} lineshape parameters for the process Z{sup 0} {r_arrow} {tau}{sup +}{tau}{sup {minus}}

    SciTech Connect

    Lahmann, R.

    1996-12-31

    In this dissertation, a measurement of the partial decay width of the process Z{sup 0} {r_arrow} {tau}{sup +}{tau}{sup {minus}} using data collected during 1993 and 1994 at the OPAL detector at CERN is described. The cross sections of this process at three center-of-mass energies near the Z{sup 0} resonance were determined, and from a fit to those cross sections, the mass of the Z{sup 0}, its total decay width and its partial decay width into {tau}{sup +}{tau}{sup {minus}} final states were determined as M{sub Z} = 91.183 {+-} 0.020 GeV, {Lambda}{sub tot} = 2.514 {+-} 0.018 GeV and {Lambda}{sub {tau}{tau}} = 84.54 {+-} 0.59 MeV. Using published results for M{sub Z}, and {Lambda}{sub tot} with higher accuracy, a value for the partial decay width of {Lambda}{sub {tau}{tau}} = 84.02 {+-} 0.20 MeV was obtained. Further using published results for the decay width of the Z{sup 0} into quark pair final states, the invisible decay width of the Z{sup 0} was determined as {Lambda}{sub inv} = 496.9 {+-} 4.1 MeV, and the number of neutrino generations was determined as N{sub {nu}} = 2.974 {+-} 0.025(exp) {+-} 0.007 (m{sub top}, M{sub Higgs}). All results were found to be in good agreement with the Standard Model predictions and were consistent with the assumption of lepton universality within the Standard Model framework.

  15. Elimination of spurious eigenvalues in the Chebyshev tau spectral method

    NASA Technical Reports Server (NTRS)

    Mcfadden, G. B.; Murray, B. T.; Boisvert, R. F.

    1990-01-01

    A very simple modification is presented for the Chebyshev tau method which can eliminate spurious eigenvalues, proceeding from a consideration of the vorticity-streamfunction reformulation of the Chebyshev tau method and the Chebyshev-Galerkin method, which have no spurious modes. Consideration of a model problem indicates that these two approaches are equivalent, and that they reduce to the present modification of the tau method. This modified tau method also eliminates spurious eigenvalues from the Orr-Sommerfeld equation.

  16. Are Tau Aggregates Toxic or Protective in Tauopathies?

    PubMed Central

    Cowan, Catherine M.; Mudher, Amrit

    2013-01-01

    Aggregation of highly phosphorylated tau into aggregated forms such as filaments and neurofibrillary tangles is one of the defining pathological hallmarks of Alzheimers disease and other tauopathies. Hence therapeutic strategies have focused on inhibition of tau phosphorylation or disruption of aggregation. However, animal models imply that tau-mediated dysfunction and toxicity do not require aggregation but instead are caused by soluble hyper-phosphorylated tau. Over the years, our findings from a Drosophila model of tauopathy have reinforced this. We have shown that highly phosphorylated wild-type human tau causes behavioral deficits resulting from synaptic dysfunction, axonal transport disruption, and cytoskeletal destabilization in vivo. These deficits are evident in the absence of neuronal death or filament/tangle formation. Unsurprisingly, both pharmacological and genetic inhibition of GSK-3? rescue these tau phenotypes. However, GSK-3? inhibition also unexpectedly increases tau protein levels, and produces insoluble granular tau oligomers. As well as underlining the growing consensus that tau toxicity is mediated by a highly phosphorylated soluble tau species, our findings further show that not all insoluble tau aggregates are toxic. Some tau aggregates, in particular tau oligomers, are non-toxic, and may even be protective against tau toxicity in vivo. This has serious implications for emerging therapeutic strategies to dissolve tau aggregates, which might be ineffective or even counter-productive. In light of this, it is imperative to identify the key toxic tau species and to understand how it mediates dysfunction and degeneration so that the effective disease-modifying therapies can be developed. PMID:23964266

  17. Tau Phosphorylation by GSK3 in Different Conditions

    PubMed Central

    Avila, Jess; Len-Espinosa, Gonzalo; Garca, Esther; Garca-Escudero, Vega; Hernndez, Flix; DeFelipe, Javier

    2012-01-01

    Almost a 20% of the residues of tau protein are phosphorylatable amino acids: serine, threonine, and tyrosine. In this paper we comment on the consequences for tau of being a phosphoprotein. We will focus on serine/threonine phosphorylation. It will be discussed that, depending on the modified residue in tau molecule, phosphorylation could be protective, in processes like hibernation, or toxic like in development of those diseases known as tauopathies, which are characterized by an hyperphosphorylation and aggregation of tau. PMID:22675648

  18. A Measurement of the charged-current interaction cross section of the tau neutrino

    SciTech Connect

    Maher, Emily O'Connor; /Minnesota U.

    2005-01-01

    The Fermilab experiment E872 (DONUT) was designed to make the first observation of the tau neutrino charged-current interaction. Using a hybrid emulsion-spectrometer detector, the tau lepton was identified by its single-prong or trident decay. Six interactions were observed, of which five were in the deep inelastic scattering region. These five interaction were used to measure the charged-current cross section of the tau neutrino. To minimize uncertainties, the tau neutrino cross section was measured relative to the electron neutrino cross section. The result {sigma}{sub {nu}{sub {tau}}N}{sup const}/{sigma}{sub {nu}{sub e}N}{sup const} = 0.77 {+-} 0.39 is consistent with 1.0, which is predicted by lepton universality. The tau neutrino cross section was also measured for 115 GeV neutrinos, which was the average energy of the interacted tau neutrinos. The result {sigma}{sub {nu}{sub {tau}}N}{sup exp} = 45 {+-} 21 x 10{sup -38} cm{sup 2} is consistent with the standard model prediction calculated in this thesis, {sigma}{sub {tau}N}{sup SM} = 48 {+-} 5 x 10{sup -38} cm{sup 2}.

  19. Enumerative Geometry, Tau-Functions and Heisenberg-Virasoro Algebra

    NASA Astrophysics Data System (ADS)

    Alexandrov, A.

    2015-08-01

    In this paper we establish relations between three enumerative geometry tau-functions, namely the Kontsevich-Witten, Hurwitz and Hodge tau-functions. The relations allow us to describe the tau-functions in terms of matrix integrals, Virasoro constraints and Kac-Schwarz operators. All constructed operators belong to the algebra (or group) of symmetries of the KP hierarchy.

  20. Antisense Reduction of Tau in Adult Mice Protects against Seizures

    PubMed Central

    DeVos, Sarah L.; Goncharoff, Dustin K.; Chen, Guo; Kebodeaux, Carey S.; Yamada, Kaoru; Stewart, Floy R.; Schuler, Dorothy R.; Maloney, Susan E.; Wozniak, David F.; Rigo, Frank; Bennett, C. Frank; Cirrito, John R.; Holtzman, David M.

    2013-01-01

    Tau, a microtubule-associated protein, is implicated in the pathogenesis of Alzheimer's Disease (AD) in regard to both neurofibrillary tangle formation and neuronal network hyperexcitability. The genetic ablation of tau substantially reduces hyperexcitability in AD mouse lines, induced seizure models, and genetic in vivo models of epilepsy. These data demonstrate that tau is an important regulator of network excitability. However, developmental compensation in the genetic tau knock-out line may account for the protective effect against seizures. To test the efficacy of a tau reducing therapy for disorders with a detrimental hyperexcitability profile in adult animals, we identified antisense oligonucleotides that selectively decrease endogenous tau expression throughout the entire mouse CNSbrain and spinal cord tissue, interstitial fluid, and CSFwhile having no effect on baseline motor or cognitive behavior. In two chemically induced seizure models, mice with reduced tau protein had less severe seizures than control mice. Total tau protein levels and seizure severity were highly correlated, such that those mice with the most severe seizures also had the highest levels of tau. Our results demonstrate that endogenous tau is integral for regulating neuronal hyperexcitability in adult animals and suggest that an antisense oligonucleotide reduction of tau could benefit those with epilepsy and perhaps other disorders associated with tau-mediated neuronal hyperexcitability. PMID:23904623

  1. Loss of Axonal Mitochondria Promotes Tau-Mediated Neurodegeneration and Alzheimer's Disease–Related Tau Phosphorylation Via PAR-1

    PubMed Central

    Iijima-Ando, Kanae; Sekiya, Michiko; Suzuki, Emiko; Lu, Bingwei; Iijima, Koichi M.

    2012-01-01

    Abnormal phosphorylation and toxicity of a microtubule-associated protein tau are involved in the pathogenesis of Alzheimer's disease (AD); however, what pathological conditions trigger tau abnormality in AD is not fully understood. A reduction in the number of mitochondria in the axon has been implicated in AD. In this study, we investigated whether and how loss of axonal mitochondria promotes tau phosphorylation and toxicity in vivo. Using transgenic Drosophila expressing human tau, we found that RNAi–mediated knockdown of milton or Miro, an adaptor protein essential for axonal transport of mitochondria, enhanced human tau-induced neurodegeneration. Tau phosphorylation at an AD–related site Ser262 increased with knockdown of milton or Miro; and partitioning defective-1 (PAR-1), the Drosophila homolog of mammalian microtubule affinity-regulating kinase, mediated this increase of tau phosphorylation. Tau phosphorylation at Ser262 has been reported to promote tau detachment from microtubules, and we found that the levels of microtubule-unbound free tau increased by milton knockdown. Blocking tau phosphorylation at Ser262 site by PAR-1 knockdown or by mutating the Ser262 site to unphosphorylatable alanine suppressed the enhancement of tau-induced neurodegeneration caused by milton knockdown. Furthermore, knockdown of milton or Miro increased the levels of active PAR-1. These results suggest that an increase in tau phosphorylation at Ser262 through PAR-1 contributes to tau-mediated neurodegeneration under a pathological condition in which axonal mitochondria is depleted. Intriguingly, we found that knockdown of milton or Miro alone caused late-onset neurodegeneration in the fly brain, and this neurodegeneration could be suppressed by knockdown of Drosophila tau or PAR-1. Our results suggest that loss of axonal mitochondria may play an important role in tau phosphorylation and toxicity in the pathogenesis of AD. PMID:22952452

  2. Riluzole rescues glutamate alterations, cognitive deficits, and tau pathology associated with P301L tau expression.

    PubMed

    Hunsberger, Holly C; Weitzner, Daniel S; Rudy, Carolyn C; Hickman, James E; Libell, Eric M; Speer, Rebecca R; Gerhardt, Greg A; Reed, Miranda N

    2015-10-01

    Hyperexcitability of the hippocampus is a commonly observed phenomenon in the years preceding a diagnosis of Alzheimer's disease (AD). Our previous work suggests a dysregulation in glutamate neurotransmission may mediate this hyperexcitability, and glutamate dysregulation correlates with cognitive deficits in the rTg(TauP301L)4510 mouse model of AD. To determine whether improving glutamate regulation would attenuate cognitive deficits and AD-related pathology, TauP301L mice were treated with riluzole (~ 12.5 mg/kg/day p.o.), an FDA-approved drug for amyotrophic lateral sclerosis that lowers extracellular glutamate levels. Riluzole-treated TauP301L mice exhibited improved performance in the water radial arm maze and the Morris water maze, associated with a decrease in glutamate release and an increase in glutamate uptake in the dentate gyrus, cornu ammonis 3 (CA3), and cornu ammonis 1 (CA1) regions of the hippocampus. Riluzole also attenuated the TauP301L-mediated increase in hippocampal vesicular glutamate transporter 1, which packages glutamate into vesicles and influences glutamate release; and the TauP301L-mediated decrease in hippocampal glutamate transporter 1, the major transporter responsible for removing glutamate from the extracellular space. The TauP301L-mediated reduction in PSD-95 expression, a marker of excitatory synapses in the hippocampus, was also rescued by riluzole. Riluzole treatment reduced total levels of tau, as well as the pathological phosphorylation and conformational changes in tau associated with the P301L mutation. These findings open new opportunities for the development of clinically applicable therapeutic approaches to regulate glutamate in vulnerable circuits for those at risk for the development of AD. PMID:26146790

  3. Trans-cellular Propagation of Tau Aggregation by Fibrillar Species*

    PubMed Central

    Kfoury, Najla; Holmes, Brandon B.; Jiang, Hong; Holtzman, David M.; Diamond, Marc I.

    2012-01-01

    Aggregation of the microtubule associated protein Tau is associated with several neurodegenerative disorders, including Alzheimer disease and frontotemporal dementia. In Alzheimer disease, Tau pathology spreads progressively throughout the brain, possibly along existing neural networks. However, it is still unclear how the propagation of Tau misfolding occurs. Intriguingly, in animal models, vaccine-based therapies have reduced Tau and synuclein pathology by uncertain mechanisms, given that these proteins are intracellular. We have previously speculated that trans-cellular propagation of misfolding could be mediated by a process similar to prion pathogenesis, in which fibrillar Tau aggregates spread pathology from cell to cell. However, there has been little evidence to demonstrate true trans-cellular propagation of Tau misfolding, in which Tau aggregates from one cell directly contact Tau protein in the recipient cell to trigger further aggregation. Here we have observed that intracellular Tau fibrils are directly released into the medium and then taken up by co-cultured cells. Internalized Tau aggregates induce fibrillization of intracellular Tau in these naive recipient cells via direct protein-protein contact that we demonstrate using FRET. Tau aggregation can be amplified across several generations of cells. An anti-Tau monoclonal antibody blocks Tau aggregate propagation by trapping fibrils in the extracellular space and preventing their uptake. Thus, propagation of Tau protein misfolding among cells can be mediated by release and subsequent uptake of fibrils that directly contact native protein in recipient cells. These results support the model of aggregate propagation by templated conformational change and suggest a mechanism for vaccine-based therapies in neurodegenerative diseases. PMID:22461630

  4. Resolved multifrequency radio observations of GG Tau

    SciTech Connect

    Andrews, Sean M.; Birnstiel, T.; Rosenfeld, K. A.; Wilner, D. J.; Chandler, Claire J.; Prez, L. M.; Isella, Andrea; Ricci, L.; Carpenter, J. M.; Calvet, N.; Corder, S. A.; Deller, A. T.; Dullemond, C. P.; Greaves, J. S.; Harris, R. J.; Henning, Th.; Linz, H.; Kwon, W.; Lazio, J.; Mundy, L. G.; and others

    2014-06-01

    We present subarcsecond resolution observations of continuum emission associated with the GG Tau quadruple star system at wavelengths of 1.3, 2.8, 7.3, and 50 mm. These data confirm that the GG Tau A binary is encircled by a circumbinary ring at a radius of 235 AU with a FWHM width of ?60 AU. We find no clear evidence for a radial gradient in the spectral shape of the ring, suggesting that the particle size distribution is spatially homogeneous on angular scales ?0.''1. A central point source, likely associated with the primary component (GG Tau Aa), exhibits a composite spectrum from dust and free-free emission. Faint emission at 7.3 mm is observed toward the low-mass star GG Tau Ba, although its origin remains uncertain. Using these measurements of the resolved, multifrequency emission structure of the GG Tau A system, models of the far-infrared to radio spectrum are developed to place constraints on the grain size distribution and dust mass in the circumbinary ring. The non-negligible curvature present in the ring spectrum implies a maximum particle size of 1-10 mm, although we are unable to place strong constraints on the distribution shape. The corresponding dust mass is 30-300 M {sub ?}, at a temperature of 20-30 K. We discuss how this significant concentration of relatively large particles in a narrow ring at a large radius might be produced in a local region of higher gas pressures (i.e., a particle 'trap') located near the inner edge of the circumbinary disk.

  5. A search for charged higgs boson decays of the top quark using hadronic decays of the tau lepton in proton-antiproton collisions at square root s = 1.8 TeV at CDF

    SciTech Connect

    L.S. Groer

    1999-01-26

    The Standard Model predicts the existence of one neutral scalar Higgs boson, which is a remnant of the mechanism that breaks the SU(2){sub L}xU(1){sub Y} electroweak symmetry and generates masses for the heavy vector bosons and fermions. Many extensions to the Standard Model predict two or more Higgs doublets, resulting in a larger spectrum of Higgs bosons including a charged Higgs boson (H{sup {+-}}). For a light charged Higgs boson mass, the top decay into a charged Higgs boson and bottom quark might occur. This thesis presents results of a direct search for this top quark decay mode via the charged Higgs decay to a tau lepton and tau-neutrino, using the hadronic decays of the tau leptons. The search data consist of 100 pb{sup -1} of Run 1 data collected between 1992-1995 at the CDF detector, from p{anti p} collisions at a center-of-mass energy of 1.8 TeV produced at Fermilab's Tevatron accelerator. A total of seven events are observed in two search channels with an expected background contribution of 7.4{+-}2.0 events coming from fake taus (5.4{+-}1.5), heavy vector boson decays with jets (1.9{+-}1.3) and dibosons(0.08{+-}0.06). Lacking evidence for a signal, we set limits on charged Higgs production at the 95% confidence level in the charged Higgs mass plane versus tan{beta}(a parameter of the theory) for a top quark mass of 175 GeV/c{sup 2} and for top production cross sections ({sigma}{sub t{anti t}}) of 5.0 and 7.5 pb, assuming the Type-II Two-Higgs-Doublet-Model. For large tan{beta}, this analysis excludes a charged Higgs boson of mass below 147(158)GeV/c{sup 2} for {sigma}{sub t{anti t}}=5.0(7.5)pb. Using the Standard Model measured top quark cross section from CDF, this limit increases to 168 GeV/c{sup 2} and we also exclude a branching fraction of top decays via this charged Higgs mode of greater than 43% for charged Higgs masses below 168 GeV/c{sup 2}.

  6. Curcumin Suppresses Soluble Tau Dimers and Corrects Molecular Chaperone, Synaptic, and Behavioral Deficits in Aged Human Tau Transgenic Mice*

    PubMed Central

    Ma, Qiu-Lan; Zuo, Xiaohong; Yang, Fusheng; Ubeda, Oliver J.; Gant, Dana J.; Alaverdyan, Mher; Teng, Edmond; Hu, Shuxin; Chen, Ping-Ping; Maiti, Panchanan; Teter, Bruce; Cole, Greg M.; Frautschy, Sally A.

    2013-01-01

    The mechanisms underlying Tau-related synaptic and cognitive deficits and the interrelationships between Tau species, their clearance pathways, and synaptic impairments remain poorly understood. To gain insight into these mechanisms, we examined these interrelationships in aged non-mutant genomic human Tau mice, with established Tau pathology and neuron loss. We also examined how these interrelationships changed with an intervention by feeding mice either a control diet or one containing the brain permeable beta-amyloid and Tau aggregate binding molecule curcumin. Transgene-dependent elevations in soluble and insoluble phospho-Tau monomer and soluble Tau dimers accompanied deficits in behavior, hippocampal excitatory synaptic markers, and molecular chaperones (heat shock proteins (HSPs)) involved in Tau degradation and microtubule stability. In human Tau mice but not control mice, HSP70, HSP70/HSP72, and HSP90 were reduced in membrane-enriched fractions but not in cytosolic fractions. The synaptic proteins PSD95 and NR2B were reduced in dendritic fields and redistributed into perikarya, corresponding to changes observed by immunoblot. Curcumin selectively suppressed levels of soluble Tau dimers, but not of insoluble and monomeric phospho-Tau, while correcting behavioral, synaptic, and HSP deficits. Treatment increased PSD95 co-immunoprecipitating with NR2B and, independent of transgene, increased HSPs implicated in Tau clearance. It elevated HSP90 and HSC70 without increasing HSP mRNAs; that is, without induction of the heat shock response. Instead curcumin differentially impacted HSP90 client kinases, reducing Fyn without reducing Akt. In summary, curcumin reduced soluble Tau and elevated HSPs involved in Tau clearance, showing that even after tangles have formed, Tau-dependent behavioral and synaptic deficits can be corrected. PMID:23264626

  7. T-Tau and P-Tau in Brain and Blood from Natural and Experimental Prion Diseases

    PubMed Central

    Rubenstein, Richard; Chang, Binggong; Petersen, Robert; Chiu, Allen; Davies, Peter

    2015-01-01

    Synaptic abnormalities are prominent in prion disease pathogenesis and are responsible for functional deficits. The microtubule associated protein, Tau, binds to and stabilizes microtubules in axons ensuring axonal transport of synaptic components. Tau phosphorylation reduces its affinity for microtubules leading to their instability and resulting in disrupted axonal transport and synaptic dysfunction. We report on the levels of total Tau (T-Tau) and phosphorylated Tau (P-Tau), measured by highly sensitive laser-based immunoassays, in the central nervous system and biofluids from experimentally transmitted prion disease in mice and natural cases of sporadic Creutzfeldt-Jakob Disease (sCJD) in humans. We found that, in contrast to sCJD where only the levels of T-Tau in brain are increased, both T-Tau and P-Tau are increased in the brains of symptomatic mice experimentally infected with the ME7, 139A and 22L mouse-adapted scrapie strains. The increased levels of T-Tau in sCJD brain, compared to control samples, were also observed in patient plasma. In contrast, there was no detectable increase in T-Tau and P-Tau in plasma from symptomatic experimentally infected mice. Furthermore, our data suggests that in mice showing clinical signs of prion disease the levels and/or ratios of T-Tau and P-Tau are only a useful parameter for differentiating the mouse-adapted scrapie strains that differ in the extent of disease. We conclude that the neuropathogenesis associated with P-Tau and synaptic dysfunction is similar for at least two of the mouse-adapted scrapie strains tested but may differ between sporadic and experimentally transmitted prion diseases. PMID:26630676

  8. Tau Oligomers Impair Artificial Membrane Integrity and Cellular Viability*

    PubMed Central

    Flach, Katharina; Hilbrich, Isabel; Schiffmann, Andrea; Gärtner, Ulrich; Krüger, Martin; Leonhardt, Marion; Waschipky, Hanka; Wick, Lukas; Arendt, Thomas; Holzer, Max

    2012-01-01

    The microtubule-associated protein Tau is mainly expressed in neurons, where it binds and stabilizes microtubules. In Alzheimer disease and other tauopathies, Tau protein has a reduced affinity toward microtubules. As a consequence, Tau protein detaches from microtubules and eventually aggregates into β-sheet-containing filaments. The fibrillization of monomeric Tau to filaments is a multistep process that involves the formation of various aggregates, including spherical and protofibrillar oligomers. Previous concepts, primarily developed for Aβ and α-synuclein, propose these oligomeric intermediates as the primary cytotoxic species mediating their deleterious effects through membrane permeabilization. In the present study, we thus analyzed whether this concept can also be applied to Tau protein. To this end, viability and membrane integrity were assessed on SH-SY5Y neuroblastoma cells and artificial phospholipid vesicles, treated with Tau monomers, Tau aggregation intermediates, or Tau fibrils. Our findings suggest that oligomeric Tau aggregation intermediates are the most toxic compounds of Tau fibrillogenesis, which effectively decrease cell viability and increase phospholipid vesicle leakage. Our data integrate Tau protein into the class of amyloidogenic proteins and enforce the hypothesis of a common toxicity-mediating mechanism for amyloidogenic proteins. PMID:23129775

  9. The disk around the brown dwarf KPNO Tau 3

    SciTech Connect

    Broekhoven-Fiene, Hannah; Matthews, Brenda; Di Francesco, James; Duchêne, Gaspard; Scholz, Aleks; Chrysostomou, Antonio; Jayawardhana, Ray

    2014-07-10

    We present submillimeter observations of the young brown dwarfs KPNO Tau 1, KPNO Tau 3, and KPNO Tau 6 at 450 μm and 850 μm taken with the Submillimetre Common-User Bolometer Array on the James Clerk Maxwell Telescope. KPNO Tau 3 and KPNO Tau 6 have been previously identified as Class II objects hosting accretion disks, whereas KPNO Tau 1 has been identified as a Class III object and shows no evidence of circumsubstellar material. Our 3σ detection of cold dust around KPNO Tau 3 implies a total disk mass of (4.0 ± 1.1) × 10{sup –4} M{sub ☉} (assuming a gas to dust ratio of 100:1). We place tight constraints on any disks around KPNO Tau 1 or KPNO Tau 6 of <2.1 × 10{sup –4} M{sub ☉} and <2.7 × 10{sup –4} M{sub ☉}, respectively. Modeling the spectral energy distribution of KPNO Tau 3 and its disk suggests the disk properties (geometry, dust mass, and grain size distribution) are consistent with observations of other brown dwarf disks and low-mass T-Tauri stars. In particular, the disk-to-host mass ratio for KPNO Tau 3 is congruent with the scenario that at least some brown dwarfs form via the same mechanism as low-mass stars.

  10. The Disk around the Brown Dwarf KPNO Tau 3

    NASA Astrophysics Data System (ADS)

    Broekhoven-Fiene, Hannah; Matthews, Brenda; Duchêne, Gaspard; Di Francesco, James; Scholz, Aleks; Chrysostomou, Antonio; Jayawardhana, Ray

    2014-07-01

    We present submillimeter observations of the young brown dwarfs KPNO Tau 1, KPNO Tau 3, and KPNO Tau 6 at 450 μm and 850 μm taken with the Submillimetre Common-User Bolometer Array on the James Clerk Maxwell Telescope. KPNO Tau 3 and KPNO Tau 6 have been previously identified as Class II objects hosting accretion disks, whereas KPNO Tau 1 has been identified as a Class III object and shows no evidence of circumsubstellar material. Our 3σ detection of cold dust around KPNO Tau 3 implies a total disk mass of (4.0 ± 1.1) × 10-4 M ⊙ (assuming a gas to dust ratio of 100:1). We place tight constraints on any disks around KPNO Tau 1 or KPNO Tau 6 of <2.1 × 10-4 M ⊙ and <2.7 × 10-4 M ⊙, respectively. Modeling the spectral energy distribution of KPNO Tau 3 and its disk suggests the disk properties (geometry, dust mass, and grain size distribution) are consistent with observations of other brown dwarf disks and low-mass T-Tauri stars. In particular, the disk-to-host mass ratio for KPNO Tau 3 is congruent with the scenario that at least some brown dwarfs form via the same mechanism as low-mass stars.

  11. APP Metabolism Regulates Tau Proteostasis in Human Cerebral Cortex Neurons

    PubMed Central

    Moore, Steven; Evans, LewisD.B.; Andersson, Therese; Portelius, Erik; Smith, James; Dias, TatyanaB.; Saurat, Nathalie; McGlade, Amelia; Kirwan, Peter; Blennow, Kaj; Hardy, John; Zetterberg, Henrik; Livesey, FrederickJ.

    2015-01-01

    Summary Accumulation of A? peptide fragments of the APP protein and neurofibrillary tangles of the microtubule-associated protein tau are the cellular hallmarks of Alzheimers disease (AD). To investigate the relationship between APP metabolism and tau protein levels and phosphorylation, we studied human-stem-cell-derived forebrain neurons with genetic forms of AD, all of which increase the release of pathogenic A? peptides. We identified marked increases in intracellular tau in genetic forms of AD that either mutated APP or increased its dosage, suggesting that APP metabolism is coupled to changes in tau proteostasis. Manipulating APP metabolism by ?-secretase and ?-secretase inhibition, as well as ?-secretase modulation, results in specific increases and decreases in tau protein levels. These data demonstrate that APP metabolism regulates tau proteostasis and suggest that the relationship between APP processing and tau is not mediated solely through extracellular A? signaling to neurons. PMID:25921538

  12. Effects of 3-repeat tau on taxol mobility through microtubules

    NASA Astrophysics Data System (ADS)

    Park, Hyunjoo; Fygenson, Deborah; Kim, Mahn Won

    2005-03-01

    Both the anti-cancer drug taxol and the microtubule-associated protein tau suppress dynamics of microtubules (MT). We have observed taxol mobility with full-length 3-repeat tau, one of six tau isoforms, using fluorescence recovery after photobleaching (FRAP) on MTs and compare with earlier results on recombinant full-length adult 4-repeat tau. Taxol mobility becomes highly sensitive to taxol concentration in the presence of 3-repeat tau (up to 1:1 molar ratio) as it does in the presence of 4-repeat tau, but is 2 to 3 times faster at low taxol concentrations. Fitting to a mean-field binding reaction model [J.L. Ross et.al, PNAS 101:12910-5 (2004)] suggests that the presence of 3-repeat tau enhances taxol movement through pores in the MT walls.

  13. Tau mediated neurodegeneration: an insight into Alzheimer's disease pathology.

    PubMed

    Obulesu, M; Venu, R; Somashekhar, R

    2011-08-01

    Extracellular accumulations of A?, hyperphosphorylation of tau and intracellular neurofibrillary tangle formation have been the hallmarks of Alzheimer's Disease (AD). Although tau and its phosphorylation play a pivotal role in the normal physiology yet its hyperphosphorylation has been a pathological manifestation in neurodegenerative disorders like AD. In this review physiology of tau, its phosphorylation, hyperphosphorylation with the intervention of various kinases, aggregation and formation of paired helical filaments has been discussed. A brief account of various animal models employed to study the pathological manifestation of tau in AD and therapeutic strategies streamlined to counter the tau induced pathology has been given. The reasons for the failure to have suitable animal model to study AD pathology and recent success in achieving this has been included. The role of caspase cascade in tau cleavage has been emphasized. The summary of current studies on tau and the need for future studies has been accentuated. PMID:21509508

  14. Tau Binds to Multiple Tubulin Dimers with Helical Structure

    PubMed Central

    Li, Xiao-Han; Culver, Jacob A.; Rhoades, Elizabeth

    2015-01-01

    Understanding the mechanism by which tau binds to and promotes microtubule (MT) assembly as part of its native function may also provide insight into its loss of function that occurs in neurodegenerative disease. Both mechanistic and structural studies of tau have been hindered by its intrinsic disorder and highly dynamic nature. Here, we combine fluorescence correlation spectroscopy and acrylodan fluorescence screening to study the stoichiometry and structural features of tau-tubulin assemblies. Our results show that tau binds to multiple tubulin dimers, even when MT assembly is inhibited. Moreover, we observe helical structure in the repeat regions of the MT binding domain of tau in the tau-tubulin complex, reflecting partial folding upon binding. Our findings support a role for taus intrinsic disorder in providing a flexible scaffold for binding tubulin and MTs and a disorder-to-order transition in mediating this important interaction. PMID:26165802

  15. Probing light pseudoscalar, axial vector states through {eta}{sub b}{yields}{tau}{sup +}{tau}{sup -}

    SciTech Connect

    Rashed, Ahmed; Duraisamy, Murugeswaran; Datta, Alakabha

    2010-09-01

    In this paper, we explore the decay {eta}{sub b}{yields}{tau}{sup +}{tau}{sup -} as a probe for a light pseudoscalar or a light axial vector state. We estimate the standard model branching ratio for this decay to be {approx}4x10{sup -9}. We show that considerably larger branching ratios, up to the present experimental limit of {approx}8%, are possible in models with a light pseudoscalar or a light axial vector state. As we do not include possible mixing effects between the light pseudoscalar and the {eta}{sub b}, our results should be reliable when the pseudoscalar mass is away from the {eta}{sub b} mass.

  16. Search for Higgs bosons predicted in two-Higgs-doublet models via decays to tau lepton pairs in 1.96-TeV p anti-p collisions

    SciTech Connect

    Aaltonen, T.; Adelman, Jahred A.; Akimoto, T.; Alvarez Gonzalez, B.; Amerio, S.; Amidei, Dante E.; Anastassov, A.; Annovi, Alberto; Antos, Jaroslav; Apollinari, G.; Apresyan, A.; /Purdue U. /Waseda U.

    2009-06-01

    We present the results of a search for Higgs bosons predicted in two-Higgs-doublet models, in the case where the Higgs bosons decay to tau lepton pairs, using 1.8 fb{sup -1} of integrated luminosity of p{bar p} collisions recorded by the CDF II experiment at the Fermilab Tevatron. Studying the mass distribution in events where one or both tau leptons decay leptonically, no evidence for a Higgs boson signal is observed. The result is used to infer exclusion limits in the two-dimensional space of tan {beta} versus m{sub A} (the ratio of the vaccum expectation values of the two Higgs doublets and the mass of the pseudoscalar boson, respectively).

  17. Search for neutral Higgs bosons decaying to tau pairs produced in association with b quarks in $$p\\bar{p}$$ collisions at $$\\sqrt{s} = 1.96$$ TeV

    DOE PAGESBeta

    Abazov, Victor Mukhamedovich

    2011-09-12

    We report results from a search for neutral Higgs bosons produced in association with b quarks using data recorded by the D0 experiment at the Fermilab Tevatron Collider and corresponding to an integrated luminosity of 7.3 fb-1. This production mode can be enhanced in several extensions of the standard model (SM) such as in its minimal supersymmetric extension (MSSM) at high tanß. We search for Higgs bosons decaying to tau pairs with one tau decaying to a muon and neutrinos and the other to hadrons. The data are found to be consistent with SM expectations, and we set upper limitsmore » on the cross section times branching ratio in the Higgs boson mass range from 90 to 320 GeV/c2. We interpret our result in the MSSM parameter space, excluding tanß values down to 25 for Higgs boson masses below 170 GeV/c2.« less

  18. Search for neutral Higgs bosons decaying to tau pairs produced in association with b quarks in $p\\bar{p}$ collisions at $\\sqrt{s} = 1.96$ TeV

    SciTech Connect

    Abazov, Victor Mukhamedovich

    2011-09-12

    We report results from a search for neutral Higgs bosons produced in association with b quarks using data recorded by the D0 experiment at the Fermilab Tevatron Collider and corresponding to an integrated luminosity of 7.3 fb-1. This production mode can be enhanced in several extensions of the standard model (SM) such as in its minimal supersymmetric extension (MSSM) at high tan. We search for Higgs bosons decaying to tau pairs with one tau decaying to a muon and neutrinos and the other to hadrons. The data are found to be consistent with SM expectations, and we set upper limits on the cross section times branching ratio in the Higgs boson mass range from 90 to 320 GeV/c2. We interpret our result in the MSSM parameter space, excluding tan values down to 25 for Higgs boson masses below 170 GeV/c2.

  19. Search for neutral minimal supersymmetric standard model Higgs bosons decaying to tau pairs produced in association with b quarks in pp collisions at ?s = 1.96 TeV.

    PubMed

    Abazov, V M; Abbott, B; Acharya, B S; Adams, M; Adams, T; Alexeev, G D; Alkhazov, G; Alton, A; Alverson, G; Alves, G A; Aoki, M; Arov, M; Askew, A; sman, B; Atramentov, O; Avila, C; BackusMayes, J; Badaud, F; Bagby, L; Baldin, B; Bandurin, D V; Banerjee, S; Barberis, E; Baringer, P; Barreto, J; Bartlett, J F; Bassler, U; Bazterra, V; Beale, S; Bean, A; Begalli, M; Begel, M; Belanger-Champagne, C; Bellantoni, L; Beri, S B; Bernardi, G; Bernhard, R; Bertram, I; Besanon, M; Beuselinck, R; Bezzubov, V A; Bhat, P C; Bhatnagar, V; Blazey, G; Blessing, S; Bloom, K; Boehnlein, A; Boline, D; Boos, E E; Borissov, G; Bose, T; Brandt, A; Brandt, O; Brock, R; Brooijmans, G; Bross, A; Brown, D; Brown, J; Bu, X B; Buehler, M; Buescher, V; Bunichev, V; Burdin, S; Burnett, T H; Buszello, C P; Calpas, B; Camacho-Prez, E; Carrasco-Lizarraga, M A; Casey, B C K; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K M; Chandra, A; Chen, G; Chevalier-Thry, S; Cho, D K; Cho, S W; Choi, S; Choudhary, B; Cihangir, S; Claes, D; Clutter, J; Cooke, M; Cooper, W E; Corcoran, M; Couderc, F; Cousinou, M-C; Croc, A; Cutts, D; Das, A; Davies, G; De, K; de Jong, S J; De La Cruz-Burelo, E; Dliot, F; Demarteau, M; Demina, R; Denisov, D; Denisov, S P; Desai, S; Deterre, C; DeVaughan, K; Diehl, H T; Diesburg, M; Ding, P F; Dominguez, A; Dorland, T; Dubey, A; Dudko, L V; Duggan, D; Duperrin, A; Dutt, S; Dyshkant, A; Eads, M; Edmunds, D; Ellison, J; Elvira, V D; Enari, Y; Evans, H; Evdokimov, A; Evdokimov, V N; Facini, G; Ferbel, T; Fiedler, F; Filthaut, F; Fisher, W; Fisk, H E; Fortner, M; Fox, H; Fuess, S; Garcia-Bellido, A; Gavrilov, V; Gay, P; Geng, W; Gerbaudo, D; Gerber, C E; Gershtein, Y; Ginther, G; Golovanov, G; Goussiou, A; Grannis, P D; Greder, S; Greenlee, H; Greenwood, Z D; Gregores, E M; Grenier, G; Gris, Ph; Grivaz, J-F; Grohsjean, A; Grnendahl, S; Grnewald, M W; Guillemin, T; Guo, F; Gutierrez, G; Gutierrez, P; Haas, A; Hagopian, S; Haley, J; Han, L; Harder, K; Harel, A; Hauptman, J M; Hays, J; Head, T; Hebbeker, T; Hedin, D; Hegab, H; Heinson, A P; Heintz, U; Hensel, C; Heredia-De La Cruz, I; Herner, K; Hesketh, G; Hildreth, M D; Hirosky, R; Hoang, T; Hobbs, J D; Hoeneisen, B; Hohlfeld, M; Hubacek, Z; Huske, N; Hynek, V; Iashvili, I; Ilchenko, Y; Illingworth, R; Ito, A S; Jabeen, S; Jaffr, M; Jamin, D; Jayasinghe, A; Jesik, R; Johns, K; Johnson, M; Johnston, D; Jonckheere, A; Jonsson, P; Joshi, J; Jung, A W; Juste, A; Kaadze, K; Kajfasz, E; Karmanov, D; Kasper, P A; Katsanos, I; Kehoe, R; Kermiche, S; Khalatyan, N; Khanov, A; Kharchilava, A; Kharzheev, Y N; Kirby, M H; Kohli, J M; Kozelov, A V; Kraus, J; Kulikov, S; Kumar, A; Kupco, A; Kur?a, T; Kuzmin, V A; Kvita, J; Lammers, S; Landsberg, G; Lebrun, P; Lee, H S; Lee, S W; Lee, W M; Lellouch, J; Li, L; Li, Q Z; Lietti, S M; Lim, J K; Lincoln, D; Linnemann, J; Lipaev, V V; Lipton, R; Liu, Y; Liu, Z; Lobodenko, A; Lokajicek, M; Lopes de Sa, R; Lubatti, H J; Luna-Garcia, R; Lyon, A L; Maciel, A K A; Mackin, D; Madar, R; Magaa-Villalba, R; Malik, S; Malyshev, V L; Maravin, Y; Martnez-Ortega, J; McCarthy, R; McGivern, C L; Meijer, M M; Melnitchouk, A; Menezes, D; Mercadante, P G; Merkin, M; Meyer, A; Meyer, J; Miconi, F; Mondal, N K; Muanza, G S; Mulhearn, M; Nagy, E; Naimuddin, M; Narain, M; Nayyar, R; Neal, H A; Negret, J P; Neustroev, P; Novaes, S F; Nunnemann, T; Obrant, G; Orduna, J; Osman, N; Osta, J; Otero y Garzn, G J; Padilla, M; Pal, A; Parashar, N; Parihar, V; Park, S K; Parsons, J; Partridge, R; Parua, N; Patwa, A; Penning, B; Perfilov, M; Peters, K; Peters, Y; Petridis, K; Petrillo, G; Ptroff, P; Piegaia, R; Pleier, M-A; Podesta-Lerma, P L M; Podstavkov, V M; Polozov, P; Popov, A V; Prewitt, M; Price, D; Prokopenko, N; Protopopescu, S; Qian, J; Quadt, A; Quinn, B; Rangel, M S; Ranjan, K; Ratoff, P N; Razumov, I; Renkel, P; Rijssenbeek, M; Ripp-Baudot, I; Rizatdinova, F; Rominsky, M; Ross, A; Royon, C; Rubinov, P; Ruchti, R; Safronov, G; Sajot, G; Salcido, P; Snchez-Hernndez, A; Sanders, M P; Sanghi, B; Santos, A S; Savage, G; Sawyer, L; Scanlon, T; Schamberger, R D; Scheglov, Y; Schellman, H; Schliephake, T; Schlobohm, S; Schwanenberger, C; Schwienhorst, R; Sekaric, J; Severini, H; Shabalina, E; Shary, V; Shchukin, A A; Shivpuri, R K; Simak, V; Sirotenko, V; Skubic, P; Slattery, P; Smirnov, D; Smith, K J; Snow, G R; Snow, J; Snyder, S; Sldner-Rembold, S; Sonnenschein, L; Soustruznik, K; Stark, J; Stolin, V; Stoyanova, D A; Strauss, M; Strom, D; Stutte, L; Suter, L; Svoisky, P; Takahashi, M; Tanasijczuk, A; Taylor, W; Titov, M; Tokmenin, V V; Tsai, Y-T; Tschann-Grimm, K; Tsybychev, D; Tuchming, B; Tully, C; Uvarov, L; Uvarov, S; Uzunyan, S; Van Kooten, R; van Leeuwen, W M; Varelas, N; Varnes, E W; Vasilyev, I A; Verdier, P; Vertogradov, L S; Verzocchi, M; Vesterinen, M; Vilanova, D; Vokac, P; Wahl, H D

    2011-09-16

    We report results from a search for neutral Higgs bosons produced in association with b quarks using data recorded by the D0 experiment at the Fermilab Tevatron Collider and corresponding to an integrated luminosity of 7.3 fb(-1). This production mode can be enhanced in several extensions of the standard model (SM) such as in its minimal supersymmetric extension (MSSM) at high tan?. We search for Higgs bosons decaying to tau pairs with one tau decaying to a muon and neutrinos and the other to hadrons. The data are found to be consistent with SM expectations, and we set upper limits on the cross section times branching ratio in the Higgs boson mass range from 90 to 320 GeV/c(2). We interpret our result in the MSSM parameter space, excluding tan? values down to 25 for Higgs boson masses below 170 GeV/c(2). PMID:22026764

  20. PE859, a Novel Tau Aggregation Inhibitor, Reduces Aggregated Tau and Prevents Onset and Progression of Neural Dysfunction In Vivo

    PubMed Central

    Okuda, Michiaki; Hijikuro, Ichiro; Fujita, Yuki; Wu, Xiaofeng; Nakayama, Shinichi; Sakata, Yoko; Noguchi, Yuji; Ogo, Makoto; Akasofu, Shigeru; Ito, Yoshimasa; Soeda, Yoshiyuki; Tsuchiya, Nobuhiko; Tanaka, Naoki; Takahashi, Takashi; Sugimoto, Hachiro

    2015-01-01

    In tauopathies, a neural microtubule-associated protein tau (MAPT) is abnormally aggregated and forms neurofibrillary tangle. Therefore, inhibition of the tau aggregation is one of the key approaches for the treatment of these diseases. Here, we have identified a novel tau aggregation inhibitor, PE859. An oral administration of PE859 resulted in the significant reduction of sarkosyl-insoluble aggregated tau along with the prevention of onset and progression of the motor dysfunction in JNPL3 P301L-mutated human tau transgenic mice. These results suggest that PE859 is useful for the treatment of tauopathies. PMID:25659102

  1. Upper limit on the diffuse flux of ultrahigh energy tau neutrinos from the Pierre Auger Observatory.

    PubMed

    Abraham, J; Abreu, P; Aglietta, M; Aguirre, C; Allard, D; Allekotte, I; Allen, J; Allison, P; Alvarez-Muiz, J; Ambrosio, M; Anchordoqui, L; Andringa, S; Anzalone, A; Aramo, C; Argir, S; Arisaka, K; Armengaud, E; Arneodo, F; Arqueros, F; Asch, T; Asorey, H; Assis, P; Atulugama, B S; Aublin, J; Ave, M; Avila, G; Bcker, T; Badagnani, D; Barbosa, A F; Barnhill, D; Barroso, S L C; Bauleo, P; Beatty, J J; Beau, T; Becker, B R; Becker, K H; Bellido, J A; BenZvi, S; Berat, C; Bergmann, T; Bernardini, P; Bertou, X; Biermann, P L; Billoir, P; Blanch-Bigas, O; Blanco, F; Blasi, P; Bleve, C; Blmer, H; Bohcov, M; Bonifazi, C; Bonino, R; Boratav, M; Brack, J; Brogueira, P; Brown, W C; Buchholz, P; Bueno, A; Burton, R E; Busca, N G; Caballero-Mora, K S; Cai, B; Camin, D V; Caramete, L; Caruso, R; Carvalho, W; Castellina, A; Catalano, O; Cataldi, G; Cazon, L; Cester, R; Chauvin, J; Chiavassa, A; Chinellato, J A; Chou, A; Chye, J; Clark, P D J; Clay, R W; Colombo, E; Conceio, R; Connolly, B; Contreras, F; Coppens, J; Cordier, A; Cotti, U; Coutu, S; Covault, C E; Creusot, A; Criss, A; Cronin, J; Curutiu, A; Dagoret-Campagne, S; Daumiller, K; Dawson, B R; de Almeida, R M; De Donato, C; de Jong, S J; De La Vega, G; de Mello Junior, W J M; de Mello Neto, J R T; DeMitri, I; de Souza, V; del Peral, L; Deligny, O; Della Selva, A; Delle Fratte, C; Dembinski, H; Di Giulio, C; Diaz, J C; Dobrigkeit, C; D'Olivo, J C; Dornic, D; Dorofeev, A; dos Anjos, J C; Dova, M T; D'Urso, D; Dutan, I; DuVernois, M A; Engel, R; Epele, L; Erdmann, M; Escobar, C O; Etchegoyen, A; Facal San Luis, P; Falcke, H; Farrar, G; Fauth, A C; Fazzini, N; Ferrer, F; Ferry, S; Fick, B; Filevich, A; Filipcic, A; Fleck, I; Fonte, R; Fracchiolla, C E; Fulgione, W; Garca, B; Garca Gmez, D; Garcia-Pinto, D; Garrido, X; Geenen, H; Gelmini, G; Gemmeke, H; Ghia, P L; Giller, M; Glass, H; Gold, M S; Golup, G; Gomez Albarracin, F; Gmez Berisso, M; Gmez Herrero, R; Gonalves, P; Gonalves do Amaral, M; Gonzalez, D; Gonzalez, J G; Gonzlez, M; Gra, D; Gorgi, A; Gouffon, P; Grassi, V; Grillo, A F; Grunfeld, C; Guardincerri, Y; Guarino, F; Guedes, G P; Gutirrez, J; Hague, J D; Hamilton, J C; Hansen, P; Harari, D; Harmsma, S; Harton, J L; Haungs, A; Hauschildt, T; Healy, M D; Hebbeker, T; Hebrero, G; Heck, D; Hojvat, C; Holmes, V C; Homola, P; Hrandel, J; Horneffer, A; Horvat, M; Hrabovsk, M; Huege, T; Hussain, M; Iarlori, M; Insolia, A; Ionita, F; Italiano, A; Kaducak, M; Kampert, K H; Karova, T; Kgl, B; Keilhauer, B; Kemp, E; Kieckhafer, R M; Klages, H O; Kleifges, M; Kleinfeller, J; Knapik, R; Knapp, J; Koang, D-H; Krieger, A; Krmer, O; Kuempel, D; Kunka, N; Kusenko, A; La Rosa, G; Lachaud, C; Lago, B L; Lebrun, D; Lebrun, P; Lee, J; Leigui de Oliveira, M A; Letessier-Selvon, A; Leuthold, M; Lhenry-Yvon, I; Lpez, R; Lopez Agera, A; Lozano Bahilo, J; Luna Garca, R; Maccarone, M C; Macolino, C; Maldera, S; Mancarella, G; Manceido, M E; Mandat, D; Mantsch, P; Mariazzi, A G; Maris, I C; Marquez Falcon, H R; Martello, D; Martnez, J; Martnez Bravo, O; Mathes, H J; Matthews, J; Matthews, J A J; Matthiae, G; Maurizio, D; Mazur, P O; McCauley, T; McEwen, M; McNeil, R R; Medina, M C; Medina-Tanco, G; Meli, A; Melo, D; Menichetti, E; Menschikov, A; Meurer, Chr; Meyhandan, R; Micheletti, M I; Miele, G; Miller, W; Mollerach, S; Monasor, M; Monnier Ragaigne, D; Montanet, F; Morales, B; Morello, C; Moreno, J C; Morris, C; Mostaf, M; Muller, M A; Mussa, R; Navarra, G; Navarro, J L; Navas, S; Necesal, P; Nellen, L; Newman-Holmes, C; Newton, D; Nguyen Thi, T; Nierstenhoefer, N; Nitz, D; Nosek, D; Nozka, L; Oehlschlger, J; Ohnuki, T; Olinto, A; Olmos-Gilbaja, V M; Ortiz, M; Ortolani, F; Ostapchenko, S; Otero, L; Pacheco, N; Pakk Selmi-Dei, D; Palatka, M; Pallotta, J; Parente, G; Parizot, E; Parlati, S; Pastor, S; Patel, M; Paul, T; Pavlidou, V; Payet, K; Pech, M; Pekala, J; Pelayo, R; Pepe, I M; Perrone, L; Petrera, S; Petrinca, P; Petrov, Y; Pham Ngoc, Diep; Pham Ngoc, Dong; Pham Thi, T N; Pichel, A; Piegaia, R; Pierog, T; Pimenta, M; Pinto, T; Pirronello, V; Pisanti, O; Platino, M; Pochon, J; Privitera, P; Prouza, M; Quel, E J; Rautenberg, J; Redondo, A; Reucroft, S; Revenu, B; Rezende, F A S; Ridky, J; Riggi, S; Risse, M; Rivire, C; Rizi, V; Roberts, M; Robledo, C; Rodriguez, G; Rodrguez Fras, D; Rodriguez Martino, J; Rodriguez Rojo, J; Rodriguez-Cabo, I; Ros, G; Rosado, J; Roth, M; Rouill-d'Orfeuil, B; Roulet, E; Rovero, A C; Salamida, F; Salazar, H; Salina, G; Snchez, F; Santander, M; Santo, C E; Santos, E M; Sarazin, F; Sarkar, S; Sato, R; Scherini, V; Schieler, H; Schmidt, A; Schmidt, F; Schmidt, T; Scholten, O; Schovnek, P; Schssler, F; Sciutto, S J; Scuderi, M; Segreto, A; Semikoz, D; Settimo, M; Shellard, R C; Sidelnik, I; Siffert, B B; Sigl, G

    2008-05-30

    The surface detector array of the Pierre Auger Observatory is sensitive to Earth-skimming tau neutrinos that interact in Earth's crust. Tau leptons from nu(tau) charged-current interactions can emerge and decay in the atmosphere to produce a nearly horizontal shower with a significant electromagnetic component. The data collected between 1 January 2004 and 31 August 2007 are used to place an upper limit on the diffuse flux of nu(tau) at EeV energies. Assuming an E(nu)(-2) differential energy spectrum the limit set at 90% C.L. is E(nu)(2)dN(nu)(tau)/dE(nu)<1.3 x 10(-7) GeV cm(-2) s(-1) sr(-1) in the energy range 2 x 10(17) eV< E(nu)< 2 x 10(19) eV. PMID:18518595

  2. Observation of the charged-current interactions of the tau neutrino

    NASA Astrophysics Data System (ADS)

    Sielaff, Jason Murray

    Fermilab experiment E872 used an emulsion detector in a tau-neutrino enriched neutrino beam to record neutrino interactions including those of the tau-neutrino. In a data set of 203 interactions located in the emulsion, four events have a signature that fulfilled tau-neutrino interaction selection criteria. The expected number of background events due to random association, charm decay and secondary interactions is 0.41 +/- 0.04. A Baysean analysis of each signal event shows the probability of all four events being due to background sources and there are no tau-neutrino interaction events in the signal is 1.4 x 10-4. This is the first observation of tau-neutrino charged-current interactions. This thesis presents the methods and results of E872.

  3. Tau Monoclonal Antibody Generation Based on Humanized Yeast Models

    PubMed Central

    Rosseels, Jolle; Van den Brande, Jeff; Violet, Marie; Jacobs, Dirk; Grognet, Pierre; Lopez, Juan; Huvent, Isabelle; Caldara, Marina; Swinnen, Erwin; Papegaey, Anthony; Caillierez, Raphalle; Bue-Scherrer, Valerie; Engelborghs, Sebastiaan; Lippens, Guy; Colin, Morvane; Bue, Luc; Galas, Marie-Christine; Vanmechelen, Eugeen; Winderickx, Joris

    2015-01-01

    A link between Tau phosphorylation and aggregation has been shown in different models for Alzheimer disease, including yeast. We used human Tau purified from yeast models to generate new monoclonal antibodies, of which three were further characterized. The first antibody, ADx201, binds the Tau proline-rich region independently of the phosphorylation status, whereas the second, ADx215, detects an epitope formed by the Tau N terminus when Tau is not phosphorylated at Tyr18. For the third antibody, ADx210, the binding site could not be determined because its epitope is probably conformational. All three antibodies stained tangle-like structures in different brain sections of THY-Tau22 transgenic mice and Alzheimer patients, and ADx201 and ADx210 also detected neuritic plaques in the cortex of the patient brains. In hippocampal homogenates from THY-Tau22 mice and cortex homogenates obtained from Alzheimer patients, ADx215 consistently stained specific low order Tau oligomers in diseased brain, which in size correspond to Tau dimers. ADx201 and ADx210 additionally reacted to higher order Tau oligomers and presumed prefibrillar structures in the patient samples. Our data further suggest that formation of the low order Tau oligomers marks an early disease stage that is initiated by Tau phosphorylation at N-terminal sites. Formation of higher order oligomers appears to require additional phosphorylation in the C terminus of Tau. When used to assess Tau levels in human cerebrospinal fluid, the antibodies permitted us to discriminate patients with Alzheimer disease or other dementia like vascular dementia, indicative that these antibodies hold promising diagnostic potential. PMID:25540200

  4. Single-molecule tracking of tau reveals fast kiss-and-hop interaction with microtubules in living neurons

    PubMed Central

    Janning, Dennis; Igaev, Maxim; Sndermann, Frederik; Brhmann, Jrg; Beutel, Oliver; Heinisch, Jrgen J.; Bakota, Lidia; Piehler, Jacob; Junge, Wolfgang; Brandt, Roland

    2014-01-01

    The microtubule-associated phosphoprotein tau regulates microtubule dynamics and is involved in neurodegenerative diseases collectively called tauopathies. It is generally believed that the vast majority of tau molecules decorate axonal microtubules, thereby stabilizing them. However, it is an open question how tau can regulate microtubule dynamics without impeding microtubule-dependent transport and how tau is also available for interactions other than those with microtubules. Here we address this apparent paradox by fast single-molecule tracking of tau in living neurons and Monte Carlo simulations of tau dynamics. We find that tau dwells on a single microtubule for an unexpectedly short time of ?40 ms before it hops to the next. This dwell time is 100-fold shorter than previously reported by ensemble measurements. Furthermore, we observed by quantitative imaging using fluorescence decay after photoactivation recordings of photoactivatable GFPtagged tubulin that, despite this rapid dynamics, tau is capable of regulating the tubulinmicrotubule balance. This indicates that tau's dwell time on microtubules is sufficiently long to influence the lifetime of a tubulin subunit in a GTP cap. Our data imply a novel kiss-and-hop mechanism by which tau promotes neuronal microtubule assembly. The rapid kiss-and-hop interaction explains why tau, although binding to microtubules, does not interfere with axonal transport. PMID:25165145

  5. Bimodal modulation of tau protein phosphorylation and conformation by extracellular Zn2+ in human-tau transfected cells.

    PubMed

    Boom, Alain; Authelet, Michle; Dedecker, Robert; Frdrick, Christelle; Van Heurck, Roxane; Daubie, Valery; Leroy, Karelle; Pochet, Roland; Brion, Jean-Pierre

    2009-06-01

    Abnormal homeostasis of heavy metals is a well-documented physiopathological mechanism in Alzheimer's disease. An exacerbation of these abnormalities is best illustrated in the amyloid plaques in Alzheimer's disease brain tissue, in which zinc reaches the enormous concentration of 1000 microM. Zinc in the plaques is thought to originate from impaired glutamatergic neurons distributed in the associative cortex and limbic structures of normal brain. Although the characteristics of zinc binding to Abeta and its role in promotion of Abeta aggregation have been intensively studied, the contribution of zinc to the development of tau pathology remains elusive. To further document the effect of zinc we have investigated the modifications of tau phosphorylation, conformation and association to microtubules induced by zinc in clonal cell lines expressing a human tau isoform. A bimodal dose dependent effect of zinc was observed. At 100 microM zinc induced a tau dephosphorylation on the PHF-1 epitope, and at higher zinc concentrations induced the appearance of the abnormal tau conformational epitope MC1 and reduced the electrophoretic mobility of tau, known to be associated to increased tau phosphorylation. High zinc concentrations also increased glycogen synthase kinase-3beta (GSK-3beta) phosphorylation on tyrosine 216, a phosphorylation associated with increased activity of this tau kinase. Live imaging of tau-EGFP expressing cells demonstrated that high zinc concentrations induced a release of tau from microtubules. These results suggest that zinc plays a significant role in the development of tau pathology associated to Alzheimer's disease. PMID:19111579

  6. Tau Ser262 phosphorylation is critical for Aβ42-induced tau toxicity in a transgenic Drosophila model of Alzheimer's disease

    PubMed Central

    Iijima, Koichi; Gatt, Anthony; Iijima-Ando, Kanae

    2010-01-01

    The amyloid-β 42 (Aβ42) peptide has been suggested to promote tau phosphorylation and toxicity in Alzheimer's disease (AD) pathogenesis; however, the underlying mechanisms are not fully understood. Using transgenic Drosophila expressing both human Aβ42 and tau, we show here that tau phosphorylation at Ser262 plays a critical role in Aβ42-induced tau toxicity. Co-expression of Aβ42 increased tau phosphorylation at AD-related sites including Ser262, and enhanced tau-induced neurodegeneration. In contrast, formation of either sarkosyl-insoluble tau or paired helical filaments was not induced by Aβ42. Co-expression of Aβ42 and tau carrying the non-phosphorylatable Ser262Ala mutation did not cause neurodegeneration, suggesting that the Ser262 phosphorylation site is required for the pathogenic interaction between Aβ42 and tau. We have recently reported that the DNA damage-activated Checkpoint kinase 2 (Chk2) phosphorylates tau at Ser262 and enhances tau toxicity in a transgenic Drosophila model. We detected that expression of Chk2, as well as a number of genes involved in DNA repair pathways, was increased in the Aβ42 fly brains. The induction of a DNA repair response is protective against Aβ42 toxicity, since blocking the function of the tumor suppressor p53, a key transcription factor for the induction of DNA repair genes, in neurons exacerbated Aβ42-induced neuronal dysfunction. Our results demonstrate that tau phosphorylation at Ser262 is crucial for Aβ42-induced tau toxicity in vivo, and suggest a new model of AD progression in which activation of DNA repair pathways is protective against Aβ42 toxicity but may trigger tau phosphorylation and toxicity in AD pathogenesis. PMID:20466736

  7. V409 Tau as Another AA Tau: Photometric Observations of Stellar Occultations by the Circumstellar Disk

    NASA Astrophysics Data System (ADS)

    Rodriguez, Joseph E.; Pepper, Joshua; Stassun, Keivan G.; Siverd, Robert J.; Cargile, Phillip; Weintraub, David A.; Beatty, Thomas G.; Gaudi, B. Scott; Mamajek, Eric E.; Sanchez, N. Nicole

    2015-07-01

    AA Tau is a well studied young stellar object (YSO) that presents many of the photometric characteristics of a Classical T Tauri star (CTTS), including short-timescale stochastic variability attributed to spots and/or accretion as well as long-duration dimming events attributed to occultations by vertical features (e.g., warps) in its circumstellar disk. We present new photometric observations of AA Tau from the Kilodegree Extremely Little Telescope North (KELT-North) which reveal a deep, extended dimming event in 2011, which we show supports the interpretation by Bouvier et al. of an occultation by a high-density feature in the circumstellar disk located \\gt 8 AU from the star. We also present KELT-North observations of V409 Tau, a relatively unstudied YSO also in TaurusAuriga, showing short timescale erratic variability, along with two separate long and deep dimming events, one from 2009 January through late 2010 October, and the other from 2012 March until at least 2013 September. We interpret both dimming events to have lasted more than 600 days, each with a depth of ?1.4 mag. From a spectral energy distribution analysis, we propose that V409 Tau is most likely surrounded by a circumstellar disk viewed nearly edge-on, and using Keplerian timescale arguments we interpret the deep dimmings of V409 Tau as occultations from one or more features within this disk ?10 AU from the star. In both AA Tau and V409 Tau, the usual CTTS short-timescale variations associated with accretion processes close to the stars continue during the occultations, further supporting the distant occulting material interpretation. Like AA Tau, V409 Tau serves as a laboratory for studying the detailed structure of the protoplanetary environments of T Tauri disks, specifically disk structures that may be signposts of planet formation at many AU out in the disk. We also provide a table of all currently known disk-occulting young stars as a convenient reference for future work on such objects.

  8. The Copernicus ultraviolet spectral atlas Tau Scorpii

    NASA Technical Reports Server (NTRS)

    Rogerson, J. B., Jr.; Upson, W. L., II

    1977-01-01

    An ultraviolet spectral atlas was presented for the B0 V star, Tau Scorpii. It was scanned from 949 to 1560 A by the Princeton spectrometer aboard the Copernicus satellite. From 949 to 1420 A the observations have a nominal resolution of 0.05 A. At the longer wavelengths, the resolution was 0.1 A. The atlas was presented in both tables and graphs.

  9. Expression, purification and crystallization of a human tau-tubulin kinase 2 that phosphorylates tau protein

    SciTech Connect

    Kitano-Takahashi, Michiko; Morita, Hiroyuki; Kondo, Shin; Tomizawa, Kayoko; Kato, Ryohei; Tanio, Michikazu; Shirota, Yoshiko; Takahashi, Hiroshi; Sugio, Shigetoshi; Kohno, Toshiyuki

    2007-07-01

    The kinase domain (residues 1331) of human tau-tubulin kinase 2 was expressed in insect cells, purified and crystallized. Diffraction data have been collected to 2.9 resolution. Tau-tubulin kinase 2 (TTBK2) is a Ser/Thr kinase that putatively phosphorylates residues Ser208 and Ser210 (numbered according to a 441-residue human tau isoform) in tau protein. Functional analyses revealed that a recombinant kinase domain (residues 1331) of human TTBK2 expressed in insect cells with a baculovirus overexpression system retains kinase activity for tau protein. The kinase domain of TTBK2 was crystallized using the hanging-drop vapour-diffusion method. The crystals belong to space group P2{sub 1}2{sub 1}2{sub 1}, with unit-cell parameters a = 55.6, b = 113.7, c = 117.3 , ? = ? = ? = 90.0. Diffraction data were collected to 2.9 resolution using synchrotron radiation at BL24XU of SPring-8.

  10. Adaptive Optics Spectroscopy of Young Stellar Jets : DG Tau, HL Tau, and RW Aur

    NASA Astrophysics Data System (ADS)

    Pyo, T.-S.; Hayashi, M.; Kobayashi, N.; Tokunaga, A. T.; Terada, H.; Takami, H.; Takato, N.; Hayashi, S. S.; Usuda, T.; Yamashita, T.; Nedachi, K.; Hayano, Y.; Kamata, Y.; Iye, M.; Gaessler, W.

    2004-05-01

    We present results of the high angular resolution spectroscopy with the near infrared [Fe II] ? 1.644 ? m emission line toward the outflows emanating from DG Tau, HL Tau, and RW Aur using the Adaptive Optics System of Subaru Telescope. We resolved the region within 140 AU (< 1'') in the vicinity of their driving sources with an angular resolution of upto 0.''16. We detected two distinct velocity components separated in space and velocity from all the objects. The high velocity component (HVC) shows the radial velocities |V| > 250 km s-1 and is extended, while the low velocity component (LVC) has the radial velocities of 80 < |V| <150 km s-1 and is located at or near the driving sources. These velocities are consistent with the interpretation that the HVC is launched from the stellar surfaces or their vicinities, while the LVC is accelerated near the inner edges of accreting disks. We also detected redshifted counter outflows for all three objects. While the redshifted outflow of RW Aur is detected within 0.''1 from the star, DG Tau and HL Tau show gaps of 0.''7 ( 100 AU) occulted by their circumstellar disks. HL Tau and RW Aur show asymmetries in velocities between their blueshifted and redshifted outflows within 1'' and 0.''1, respectively, from the stars. We have demonstrated that the [Fe II] spectroscopy at high spatial and velocity resolutions is a powerful tool to study the outflow mechanisms from young stellar objects especially with large extinctions.

  11. Chaperones increase association of tau protein with microtubules

    PubMed Central

    Dou, Fei; Netzer, William J.; Tanemura, Kentaro; Li, Feng; Hartl, F. Ulrich; Takashima, Akihiko; Gouras, Gunnar K.; Greengard, Paul; Xu, Huaxi

    2003-01-01

    Molecular chaperones and their functions in protein folding have been implicated in several neurodegenerative diseases, including Parkinson's disease and Huntington's disease, which are characterized by accumulation of protein aggregates (e.g., ?-synuclein and huntingtin, respectively). These aggregates have been shown in various experimental systems to respond to changes in levels of molecular chaperones suggesting the possibility of therapeutic intervention and a role for chaperones in disease pathogenesis. It remains unclear whether chaperones also play a role in Alzheimer's disease, a neurodegenerative disorder characterized by ?-amyloid and tau protein aggregates. Here, we report an inverse relationship between aggregated tau and the levels of heat shock protein (Hsp)70/90 in tau transgenic mouse and Alzheimer's disease brains. In various cellular models, increased levels of Hsp70 and Hsp90 promote tau solubility and tau binding to microtubules, reduce insoluble tau and cause reduced tau phosphorylation. Conversely, lowered levels of Hsp70 and Hsp90 result in the opposite effects. We have also demonstrated a direct association of the chaperones with tau proteins. Our results suggest that up-regulation of molecular chaperones may suppress formation of neurofibrillary tangles by partitioning tau into a productive folding pathway and thereby preventing tau aggregation. PMID:12522269

  12. Can numerical modeling help understand the fate of tau protein in the axon terminal?

    PubMed

    Kuznetsov, I A; Kuznetsov, A V

    2016-02-01

    In this paper, we used mathematical modeling to investigate the fate of tau protein in the axon terminal. We developed a comprehensive model of tau transport that accounts for transport of cytosolic tau by diffusion, diffusion transport of microtubule (MT)-bound tau along the MT lattice, active motor-driven transport of MT-bound tau via slow axonal transport mechanism, and degradation of tau in the axon due to tau's finite half-life. We investigated the effect of different assumptions concerning the fate of tau in the terminal on steady-state transport of tau in the axon. In particular, we studied two possible scenarios: (i) tau is destroyed in the terminal and (ii) there is no tau destruction in the terminal, and to avoid tau accumulation we postulated zero flux of tau at the terminal. We found that the tau concentration and percentage of MT-bound tau are not very sensitive to the assumption concerning the fate of tau in the terminal, but the tau's flux and average velocity of tau transport are very sensitive to this assumption. This suggests that measuring the velocity of tau transport and comparing it with the results of mathematical modeling for different assumptions concerning tau's fate in the terminal can provide information concerning what happens to tau in the terminal. PMID:25563412

  13. Hsc70 Rapidly Engages Tau after Microtubule Destabilization*

    PubMed Central

    Jinwal, Umesh K.; O'Leary, John C.; Borysov, Sergiy I.; Jones, Jeffrey R.; Li, Qingyou; Koren, John; Abisambra, Jose F.; Vestal, Grant D.; Lawson, Lisa Y.; Johnson, Amelia G.; Blair, Laura J.; Jin, Ying; Miyata, Yoshinari; Gestwicki, Jason E.; Dickey, Chad A.

    2010-01-01

    The microtubule-associated protein Tau plays a crucial role in regulating the dynamic stability of microtubules during neuronal development and synaptic transmission. In a group of neurodegenerative diseases, such as Alzheimer disease and other tauopathies, conformational changes in Tau are associated with the initial stages of disease pathology. Folding of Tau into the MC1 conformation, where the amino acids at residues 79 interact with residues 312342, is one of the earliest pathological alterations of Tau in Alzheimer disease. The mechanism of this conformational change in Tau and the subsequent effect on function and association to microtubules is largely unknown. Recent work by our group and others suggests that members of the Hsp70 family play a significant role in Tau regulation. Our new findings suggest that heat shock cognate (Hsc) 70 facilitates Tau-mediated microtubule polymerization. The association of Hsc70 with Tau was rapidly enhanced following treatment with microtubule-destabilizing agents. The fate of Tau released from the microtubule was found to be dependent on ATPase activity of Hsc70. Microtubule destabilization also rapidly increased the MC1 folded conformation of Tau. An in vitro assay suggests that Hsc70 facilitates formation of MC1 Tau. However, in a hyperphosphorylating environment, the formation of MC1 was abrogated, but Hsc70 binding to Tau was enhanced. Thus, under normal circumstances, MC1 formation may be a protective conformation facilitated by Hsc70. However, in a diseased environment, Hsc70 may preserve Tau in a more unstructured state, perhaps facilitating its pathogenicity. PMID:20308058

  14. Measurement of the Tau Lepton Lifetime Using the SLD Detector at the Stanford Linear Collider

    SciTech Connect

    Turk, J

    2004-01-05

    The lifetime of the tau lepton is measured to be (2.50 {+-} 0.35) x 10{sup -14}s. The measurement combines the results of two different techniques used on separate samples of tau events collected at the Stanford Linear Collider by the SLD detector during the 1992 physics run. The first technique measures the decay length from the known interaction position to the reconstructed decay vertex position. This requires that the taus have at least three charged decay products. The second technique infers the decay length by correlating the differences in signed impact parameters (for single-charged track decays) with the angles between the tracks.

  15. Measurement of Tau branching ratios

    NASA Astrophysics Data System (ADS)

    Decamp, D.; Deschizeaux, B.; Goy, C.; Lees, J.-P.; Minard, M.-N.; Alemany, R.; Crespo, J. M.; Delfino, M.; Fernandez, E.; Gaitan, V.; Garrido, Ll.; Mir, Ll. M.; Pacheco, A.; Catanesi, M. G.; Creanza, D.; de Palma, M.; Farilla, A.; Iaselli, G.; Maggi, G.; Maggi, M.; Natali, S.; Nuzzo, S.; Quattromini, M.; Ranieri, A.; Raso, G.; Romano, F.; Ruggieri, F.; Selvaggi, G.; Silvestris, L.; Tempesta, P.; Zito, G.; Hu, H.; Huang, D.; Huang, X.; Lin, J.; Lou, J.; Qiao, C.; Ruan, T.; Wang, T.; Xie, Y.; Xu, D.; Xu, R.; Zhang, J.; Zhao, W.; Atwood, W. B.; Bauerdick, L. A. T.; Bird, F.; Blucher, E.; Bonvicini, G.; Bossi, F.; Boudreau, J.; Burnett, T. H.; Drevermann, H.; Forty, R. W.; Grab, C.; Hagelberg, R.; Haywood, S.; Hilgart, J.; Jost, B.; Kasemann, M.; Knobloch, J.; Lacourt, A.; Lanon, E.; Lehraus, I.; Lohse, T.; Lusiani, A.; Marchioro, A.; Martinez, M.; Mato, P.; Menary, S.; Meyer, T.; Minten, A.; Miotto, A.; Miquel, R.; Moser, H.-G.; Nash, J.; Palazzi, P.; Ranjard, F.; Redlinger, G.; Rolandi, L.; Roth, A.; Rothberg, J.; Saich, M.; Schlatter, D.; Schmelling, M.; Tejessy, W.; Wachsmuth, H.; Wasserbaech, S.; Wiedenmann, W.; Witzeling, W.; Wotschack, J.; Ajaltouni, Z.; Badaud, F.; Bardadin-Otwinowska, M.; Bencheikh, A. M.; El Fellous, R.; Falvard, A.; Gay, P.; Guicheney, C.; Henrard, P.; Jousset, J.; Michel, B.; Montret, J.-C.; Pallin, D.; Perret, P.; Pietrzyk, B.; Proriol, J.; Prulhire, F.; Stimpfl, G.; Hansen, J. D.; Hansen, J. R.; Hansen, P. H.; Mllerud, R.; Nilsson, B. S.; Efthymiopoulos, I.; Simopoulos, E.; Vayaki, A.; Badier, J.; Blondel, A.; Bonneaud, G.; Brient, J. C.; Fouque, G.; Gamess, A.; Harvey, J.; Orteu, S.; Rosowsky, A.; Roug, A.; Rumpf, M.; Tanaka, R.; Videau, H.; Candlin, D. J.; Veitch, E.; Moneta, L.; Parrini, G.; Corden, M.; Georgiopoulos, C.; Ikeda, M.; Lannutti, J.; Levinthal, D.; Mermikides, M.; Sawyer, L.; Antonelli, A.; Baldini, R.; Bencivenni, G.; Bologna, G.; Campana, P.; Capon, G.; Cerutti, F.; Chiarella, V.; D'Ettore-Piazzoli, B.; Felici, G.; Laurelli, P.; Mannocchi, G.; Murtas, F.; Murtas, G. P.; Passalacqua, L.; Pepe-Altarelli, M.; Picchi, P.; Zografou, P.; Altoon, B.; Boyle, O.; Colrain, P.; Halley, A. W.; Ten Have, I.; Lynch, J. G.; Maitland, W.; Morton, W. T.; Raine, C.; Scarr, J. M.; Smith, K.; Thompson, A. S.; Turnbull, R. M.; Brandl, B.; Braun, O.; Geiges, R.; Geweniger, C.; Hanke, P.; Hepp, V.; Kluge, E. E.; Maumary, Y.; Putzer, A.; Rensch, B.; Stahl, A.; Tittel, K.; Wunsch, M.; Belk, A. T.; Beuselinck, R.; Binnie, D. M.; Cameron, W.; Cattaneo, M.; Dornan, P. J.; Dugeay, S.; Greene, A. M.; Hassard, J. F.; Lieske, N. M.; Patton, S. J.; Payne, D. G.; Phillips, M. J.; Sedgbeer, J. K.; Taylor, G.; Tomalin, I. R.; Wright, A. G.; Girtler, P.; Kuhn, D.; Rudolph, G.; Bowdery, C. K.; Broodbeck, T. J.; Finch, A. J.; Foster, F.; Hughes, G.; Jackson, D.; Keemer, N. R.; Nuttall, M.; Patel, A.; Sloan, T.; Snow, S. W.; Whelan, E. P.; Barczewski, T.; Kleinknecht, K.; Raab, J.; Renk, B.; Roehn, S.; Sander, H.-G.; Schmidt, H.; Steeg, F.; Walther, S. M.; Wolf, B.; Aubert, J.-J.; Benchouk, C.; Bernard, V.; Bonissent, A.; Carr, J.; Coyle, P.; Drinkhard, J.; Etienne, F.; Papalexiou, S.; Payre, P.; Qian, Z.; Rousseau, D.; Schwemling, P.; Talby, M.; Adlung, S.; Becker, H.; Blum, W.; Brown, D.; Cattaneo, P.; Cowan, G.; Dehning, B.; Dietl, H.; Dydak, F.; Fernandez-Bosman, M.; Hansl-Kosanecka, T.; Jahn, A.; Kozanecki, W.; Lange, E.; Lauber, J.; Ltjens, G.; Lutz, G.; Mnner, W.; Richter, R.; Rotscheidt, H.; Schrder, J.; Schwarz, A. S.; Settles, R.; Stierlin, U.; Stiegler, U.; Denis, R. St.; Takashima, M.; Thomas, J.; Wolf, G.; Bertin, V.; Boucrot, J.; Callot, O.; Chen, X.; Cordier, A.; Davier, M.; Grivaz, J.-F.; Heusse, Ph.; Janot, P.; Kim, D. W.; Le Diberder, F.; Lefranois, J.; Lutz, A.-M.; Schune, M.-H.; Veillet, J.-J.; Videau, I.; Zhang, Z.; Zomer, F.; Abbaneo, D.; Amendolia, S. R.; Bagliesi, G.; Batignani, G.; Bosisio, L.; Bottigli, U.; Bradaschia, C.; Carpinelli, M.; Ciocci, M. A.; Dell'Orso, R.; Ferrante, I.; Fidecaro, F.; Fo, L.; Focardi, E.; Forti, F.; Gatto, C.; Grassi, A.; Giorgi, M. A.; Ligabue, F.; Mannelli, E. B.; Marrocchesi, P. S.; Messineo, A.; Palla, F.; Sanguinetti, G.; Steinberger, J.; Tenchini, R.; Tonelli, G.; Triggiani, G.; Vannini, C.; Venturi, A.; Verdini, P. G.; Walsh, J.; Carter, J. M.; Green, M. G.; March, P. V.; Medcalf, T.; Quasi, I. S.; Strong, J. A.; West, L. R.; Wildish, T.; Botterill, D. R.; Clifft, R. W.; Edgecock, T. R.; Edwards, M.; Fisher, S. M.; Jones, T. J.; Norton, P. R.; Salmon, D. P.; Thompson, J. C.; Bloch-Devaux, B.; Colas, P.; Locci, E.; Loucatos, S.; Monnier, E.; Perez, P.; Perlas, J. A.; Perrier, F.; Rander, J.; Renardy, J.-F.; Roussarie, A.; Schuller, J.-P.; Schwindling, J.; Vallage, B.; Ashman, J. G.; Booth, C. N.; Buttar, C.; Carney, R. E.

    1992-06-01

    Using the data accumulated at LEP in 1989 and 1990 with the ALEPH detector, the inclusive and exclusive branching ratios of the ? lepton have been measured assuming lepton universality in Z 0 decays. The inclusive branching fractions for the ? decay into one, three, and five charged particles have been determined to be (85.450.97)%, (14.350.48)%, and (0.100.05)%, respectively, in agreement with the world averages. New undetected decay modes are determined to have a branching fraction of less than 2.1% at 95% CL. The measured branching ratios for quasi-exclusive channels are slightly larger than, but consistent with the world averages, except for the modes ??3 hadrons+ v ? and ??hadron+2?0 v ? , which are significantly larger. These latter branching ratios have been found to be (9.50.7)% and (10.21.1)%, respectively. The sum of all the measured quasi-exclusive branching ratios is (100.41.8)%. A fully exclusive analysis of modes with neutral pions shows no evidence for new photonic decay modes with a branching fraction limit of 3.4% at 95% CL.

  16. Polymeric alkylpyridinium salts permit intracellular delivery of human Tau in rat hippocampal neurons: requirement of Tau phosphorylation for functional deficits.

    PubMed

    Koss, Dave J; Robinson, Lianne; Mietelska-Porowska, Anna; Gasiorowska, Anna; Sep?i?, Kristina; Turk, Tom; Jaspars, Marcel; Niewiadomska, Grazyna; Scott, Roderick H; Platt, Bettina; Riedel, Gernot

    2015-12-01

    Patients suffering from tauopathies including frontotemporal dementia (FTD) and Alzheimer's disease (AD) present with intra-neuronal aggregation of microtubule-associated protein Tau. During the disease process, Tau undergoes excessive phosphorylation, dissociates from microtubules and aggregates into insoluble neurofibrillary tangles (NFTs), accumulating in the soma. While many aspects of the disease pathology have been replicated in transgenic mouse models, a region-specific non-transgenic expression model is missing. Complementing existing models, we here report a novel region-specific approach to modelling Tau pathology. Local co-administration of the pore-former polymeric 1,3-alkylpyridinium salts (Poly-APS) extracted from marine sponges, and synthetic full-length 4R recombinant human Tau (hTau) was performed in vitro and in vivo. At low doses, Poly-APS was non-toxic and cultured cells exposed to Poly-APS (0.5g/ml) and hTau (1g/ml;~22M) had normal input resistance, resting-state membrane potentials and Ca(2+) transients induced either by glutamate or KCl, as did cells exposed to a low concentration of the phosphatase inhibitor Okadaic acid (OA; 1nM, 24h). Combined hTau loading and phosphatase inhibition resulted in a collapse of the membrane potential, suppressed excitation and diminished glutamate and KCl-stimulated Ca(2+) transients. Stereotaxic infusions of Poly-APS (0.005g/ml) and hTau (1g/ml) bilaterally into the dorsal hippocampus at multiple sites resulted in hTau loading of neurons in rats. A separate cohort received an additional 7-day minipump infusion of OA (1.2nM) intrahippocampally. When tested 2weeks after surgery, rats treated with Poly-APS+hTau+OA presented with subtle learning deficits, but were also impaired in cognitive flexibility and recall. Hippocampal plasticity recorded from slices ex vivo was diminished in Poly-APS+hTau+OA subjects, but not in other treatment groups. Histological sections confirmed the intracellular accumulation of hTau in CA1 pyramidal cells and along their processes; phosphorylated Tau was present only within somata. This study demonstrates that cognitive, physiological and pathological symptoms reminiscent of tauopathies can be induced following non-mutant hTau delivery into CA1 in rats, but functional consequences hinge on increased Tau phosphorylation. Collectively, these data validate a novel model of locally infused recombinant hTau protein as an inducer of Tau pathology in the hippocampus of normal rats; future studies will provide insights into the pathological spread and maturation of Tau pathology. PMID:26070304

  17. The CDF-II tau physics program triggers, tau ID and preliminary results

    SciTech Connect

    C. Pagliarone et al.

    2003-11-03

    The study of processes containing {tau} leptons in the final state will play an important role at Tevatron Run II. Such final states will be relevant both for electroweak studies and measurements as well as in searches for physics beyond the Standard Model. The present paper discusses the physics opportunities and challenges related to the implementation of new set of triggers able to select events containing tau candidates in the final state. They illustrate, in particular, the physics capabilities for a variety of new physics scenarios such as supersymmetry (SUSY), SUSY with Rp-parity violation, with Bilinear parity violation or models with the violation of lepton flavor. Finally, they present the first Run II results obtained using some of the described tau triggers.

  18. UV and optical spectrum variability of T Tau and RY Tau

    NASA Astrophysics Data System (ADS)

    Ismailov, N. Z.; Quliyev, N. Kh.; Khalilov, O. V.; Adigezalzade, H. N.

    2013-03-01

    In this report we have presented results of spectral observations of classical T Tauri type stars T Tau and RY Tau. Observational dates were obtained from following sources: spectrograms of the UV range from the IUE archive data, and spectrograms of the visual range obtained in the 2 m telescope of ShAO of the NAS of Azerbaijan (Ismailov et al. 2010). For both of stars on the Scargle method we have searched a periodicity of variations in equivalent widths of emission lines in the optical and UV ranges. In the RY Tau firstly was detected the periodic variability in MgII ?2800 emission doublet intensities with a period of 23 days. The observed period had also revealed with the equivalent widths and displacements of components of H? and H+H? and K CaII emission.

  19. The {tau}-contamination in the golden channel at the Neutrino Factory

    SciTech Connect

    Coloma, Pilar

    2011-10-06

    Experimental results could lead to wrong measurements of the neutrino oscillation parameters if the so-called {tau}-contamination is not properly taken into account in the data analysis. It was shown in [1] that, if a migration matrix giving the energy distribution of muon neutrinos coming from tau-decays in the detector is included, the analysis can be done in the reconstructed neutrino energy and the problem is solved for the golden channel. We will also present some preliminary results for the disappearance channel, where the {tau}-contamination is more severe.

  20. Search for Second-Class Currents in \\tau^-\\to\\omega\\pi^-\

    SciTech Connect

    Aubert, Bernard; Bona, M.; Karyotakis, Y.; Lees, J.P.; Poireau, V.; Prencipe, E.; Prudent, X.; Tisserand, V.; Garra Tico, J.; Grauges, E.; Lopez, L.; Palano, Antimo; Pappagallo, M.; Eigen, G.; Stugu, Bjarne; Sun, L.; Abrams, G.S.; Battaglia, M.; Brown, D.N.; Cahn, Robert N.; Jacobsen, R.G.; /LBL, Berkeley /Birmingham U. /Ruhr U., Bochum /Bristol U. /British Columbia U. /Brunel U. /Novosibirsk, IYF /UC, Irvine /UCLA /UC, Riverside /UC, San Diego /UC, Santa Barbara /UC, Santa Cruz /Caltech /Cincinnati U. /Colorado U. /Colorado State U. /Dortmund U. /Dresden, Tech. U. /Ecole Polytechnique /Edinburgh U. /Ferrara U. /INFN, Ferrara /Frascati /Genoa U. /INFN, Genoa /Harvard U. /Heidelberg U. /Humboldt U., Berlin /Imperial Coll., London /Iowa U. /Iowa State U. /Johns Hopkins U. /Orsay, LAL /LLNL, Livermore /Liverpool U. /Queen Mary, U. of London /Royal Holloway, U. of London /Louisville U. /Mainz U., Inst. Kernphys. /Manchester U. /Maryland U. /Massachusetts U., Amherst /MIT /McGill U. /Consorzio Milano Ricerche /INFN, Milan /Mississippi U. /Montreal U. /Mt. Holyoke Coll. /Napoli Seconda U. /INFN, Naples /NIKHEF, Amsterdam /Notre Dame U. /Ohio State U. /Oregon U. /Padua U. /INFN, Padua /Paris U., VI-VII /Pennsylvania U. /Perugia U. /INFN, Perugia /INFN, Pisa /Princeton U. /Banca di Roma /Frascati /Rostock U. /Rutherford /DAPNIA, Saclay /South Carolina U. /SLAC /Stanford U., Phys. Dept. /SUNY, Albany /Tennessee U. /Texas U. /Texas U., Dallas /Turin U. /INFN, Turin /Trieste U. /INFN, Trieste /Valencia U., IFIC /Victoria U. /Warwick U. /Wisconsin U., Madison

    2008-09-03

    We report on an analysis of {tau}{sup -} decaying into {omega}{pi}{sup -}{nu}{sub {tau}} with {omega} {yields} {pi}{sup +}{pi}{sup -}{pi}{sup 0} using data containing nearly 320 million tau pairs collected with the BABAR detector at the PEP-II asymmetric energy B-Factory. We find no evidence for second-class currents and set an upper limit at 0.69% at a 90% confidence level for the ratio of second- to first-class currents.

  1. Physics of a high luminosity collider operated near charm and tau pair thresholds

    SciTech Connect

    Schindler, R.H.

    1989-06-01

    The current plans for a high luminosity e/sup +/e/sup /minus// collider between 3.0 and 4.4 GeV/c/sup 2/ are described. Such a dedicated facility (The Tau-Charm Factory), operating near tau-pair and charm thresholds would allow studies of the decay of the third generation tau-lepton and the second generation c-quark with unprecedented precision and control of systematics. The charm physics of such a facility is discussed. 24 refs., 4 figs., 7 tabs.

  2. Tau contributions to muon/electron events at a neutrino factory

    SciTech Connect

    Sinha, Nita

    2011-10-06

    The oscillation of the muon and electron neutrinos (anti-neutrinos) to tau neutrinos (anti-neutrinos) adds to the muon and electron events sample (both right sign and wrong sign) via leptonic decays of the taus produced through charge current interactions in the detector. We focus on how this contribution affects a precision measurement of the atmospheric mixing parameters and the deviation of v{sub {mu}} {r_reversible} v{sub {tau}} mixing from maximality. We also comment on the tau contamination in the golden and platinum channels.

  3. Distinct FTDP-17 Missense Mutations in Tau Produce Tau Aggregates and Other Pathological Phenotypes in Transfected CHO Cells

    PubMed Central

    Vogelsberg-Ragaglia, Vanessa; Bruce, Jennifer; Richter-Landsberg, Christiane; Zhang, Bin; Hong, Ming; Trojanowski, John Q.; Lee, Virginia M.-Y.

    2000-01-01

    Multiple tau gene mutations are pathogenic for hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), with filamentous tau aggregates as the major lesions in the CNS of these patients. Recent studies have shown that bacterially expressed recombinant tau proteins with FTDP-17 missense mutations cause functional impairments, i.e., a reduced ability of mutant tau to bind to or promote the assembly of microtubules. To investigate the biological consequences of FTDP-17 tau mutants and assess their ability to form filamentous aggregates, we engineered Chinese hamster ovary cell lines to stably express tau harboring one or several different FTDP-17 mutations and showed that different tau mutants produced distinct pathological phenotypes. For example, ΔK, but not several other single tau mutants (e.g., V337 M, P301L, R406W), developed insoluble amorphous and fibrillar aggregates, whereas a triple tau mutant (VPR) containing V337M, P301L, and R406W substitutions also formed similar aggregates. Furthermore, the aggregates increased in size over time in culture. Significantly, the formation of aggregated ΔK and VPR tau protein correlated with reduced affinity of these mutants to bind microtubules. Reduced phosphorylation and altered proteolysis was also observed in R406W and ΔK tau mutants. Thus, distinct pathological phenotypes, including the formation of insoluble filamentous tau aggregates, result from the expression of different FTDP-17 tau mutants in transfected Chinese hamster ovary cells and implies that these missense mutations cause diverse neurodegenerative FTDP-17 syndromes by multiple mechanisms. PMID:11102510

  4. Distinct FTDP-17 missense mutations in tau produce tau aggregates and other pathological phenotypes in transfected CHO cells.

    PubMed

    Vogelsberg-Ragaglia, V; Bruce, J; Richter-Landsberg, C; Zhang, B; Hong, M; Trojanowski, J Q; Lee, V M

    2000-12-01

    Multiple tau gene mutations are pathogenic for hereditary frontotemporal dementia and parkinsonism linked to chromosome 17 (FTDP-17), with filamentous tau aggregates as the major lesions in the CNS of these patients. Recent studies have shown that bacterially expressed recombinant tau proteins with FTDP-17 missense mutations cause functional impairments, i.e., a reduced ability of mutant tau to bind to or promote the assembly of microtubules. To investigate the biological consequences of FTDP-17 tau mutants and assess their ability to form filamentous aggregates, we engineered Chinese hamster ovary cell lines to stably express tau harboring one or several different FTDP-17 mutations and showed that different tau mutants produced distinct pathological phenotypes. For example, delta K, but not several other single tau mutants (e.g., V337 M, P301L, R406W), developed insoluble amorphous and fibrillar aggregates, whereas a triple tau mutant (VPR) containing V337M, P301L, and R406W substitutions also formed similar aggregates. Furthermore, the aggregates increased in size over time in culture. Significantly, the formation of aggregated delta K and VPR tau protein correlated with reduced affinity of these mutants to bind microtubules. Reduced phosphorylation and altered proteolysis was also observed in R406W and delta K tau mutants. Thus, distinct pathological phenotypes, including the formation of insoluble filamentous tau aggregates, result from the expression of different FTDP-17 tau mutants in transfected Chinese hamster ovary cells and implies that these missense mutations cause diverse neurodegenerative FTDP-17 syndromes by multiple mechanisms. PMID:11102510

  5. The Role of Tau in Alzheimer's Disease and Related Disorders

    PubMed Central

    Medeiros, Rodrigo; Baglietto-Vargas, David; LaFerla, Frank M.

    2014-01-01

    Tau, the microtubule-associated protein, forms insoluble filaments that accumulate as neurofibrillary tangles in Alzheimer's disease (AD) and related tauopathies. Under physiological conditions, tau regulates the assembly and maintenance of the structural stability of microtubules. In the diseased brain, however, tau becomes abnormally hyperphosphorylated, which ultimately causes the microtubules to disassemble, and the free tau molecules aggregate into paired helical filaments. A large body of evidence suggests that tau hyperphosphorylation results from perturbation of cellular signaling, mainly through imbalance in the activities of different protein kinases and phosphatases. In AD, it appears that A plays a pivotal role in triggering this imbalance. In this review, we summarize our current understanding of the role of tau in AD and other tauopathies, and highlight key issues that need to be addressed to improve the success of developing novel therapies. PMID:20553310

  6. PET Imaging of Tau Deposition in the Aging Human Brain.

    PubMed

    Schöll, Michael; Lockhart, Samuel N; Schonhaut, Daniel R; O'Neil, James P; Janabi, Mustafa; Ossenkoppele, Rik; Baker, Suzanne L; Vogel, Jacob W; Faria, Jamie; Schwimmer, Henry D; Rabinovici, Gil D; Jagust, William J

    2016-03-01

    Tau pathology is a hallmark of Alzheimer's disease (AD) but also occurs in normal cognitive aging. Using the tau PET agent (18)F-AV-1451, we examined retention patterns in cognitively normal older people in relation to young controls and AD patients. Age and β-amyloid (measured using PiB PET) were differentially associated with tau tracer retention in healthy aging. Older age was related to increased tracer retention in regions of the medial temporal lobe, which predicted worse episodic memory performance. PET detection of tau in other isocortical regions required the presence of cortical β-amyloid and was associated with decline in global cognition. Furthermore, patterns of tracer retention corresponded well with Braak staging of neurofibrillary tau pathology. The present study defined patterns of tau tracer retention in normal aging in relation to age, cognition, and β-amyloid deposition. PMID:26938442

  7. Tau as a therapeutic target in neurodegenerative disease

    PubMed Central

    Himmelstein, Diana S.; Ward, Sarah M.; Lancia, Jody K.; Patterson, Kristina R.

    2013-01-01

    Tau is a microtubule-associated protein thought to help modulate the stability of neuronal microtubules. In tauopathies, including Alzheimer’s disease and several frontotemporal dementias, tau is abnormally modified and misfolded resulting in its disassociation from microtubules and the generation of pathological lesions characteristic for each disease. A recent surge in the population of people with neurodegenerative tauopathies has highlighted the immense need for disease-modifying therapies for these conditions, and new attention has focused on tau as a potential target for intervention. In the current work we summarize evidence linking tau to disease pathogenesis and review recent therapeutic approaches aimed at ameliorating tau dysfunction. The primary therapeutic tactics considered include kinase inhibitors and phosphatase activators, immunotherapies, small molecule inhibitors of protein aggregation, and microtubule-stabilizing agents. Although the evidence for tau-based treatments is encouraging, additional work is undoubtedly needed to optimize each treatment strategy for the successful development of safe and effective therapeutics. PMID:22790092

  8. A precise measurement of the tau polarization and its forward-backward asymmetry at LEP

    NASA Astrophysics Data System (ADS)

    Alexander, G.; Allison, J.; Altekamp, N.; Ametewee, K.; Anderson, K. J.; Anderson, S.; Arcelli, S.; Asai, S.; Axen, D.; Azuelos, G.; Ball, A. H.; Barberio, E.; Barlow, R. J.; Bartoldus, R.; Batley, J. R.; Beaudoin, G.; Bechtluft, J.; Beeston, C.; Behnke, T.; Bell, A. N.; Bell, K. W.; Bella, G.; Bentvelsen, S.; Berlich, P.; Bethke, S.; Biebel, O.; Blobel, V.; Bloodworth, I. J.; Bloomer, J. E.; Bock, P.; Bosch, H. M.; Boutemeur, M.; Bouwens, B. T.; Braibant, S.; Brown, R. M.; Burckhart, H. J.; Burgard, C.; Brgin, R.; Capiluppi, P.; Carnegie, R. K.; Carter, A. A.; Carter, J. R.; Chang, C. Y.; Charlesworth, C.; Charlton, D. G.; Chrisman, D.; Chu, S. L.; Clarke, P. E. L.; Cohen, I.; Conboy, J. E.; Cooke, O. C.; Cuffiani, M.; Dado, S.; Dallapiccola, C.; Dallavalle, G. M.; de Jong, S.; Del Pozo, L. A.; Desch, K.; Dixit, M. S.; Do Couto E Silva, E.; Doucet, M.; Duchovni, E.; Duckeck, G.; Duerdoth, I. P.; Edwards, J. E. G.; Estabrooks, P. G.; Evans, H. G.; Evans, M.; Fabbri, F.; Fath, P.; Fiedler, F.; Fierro, M.; Fischer, H. M.; Folman, R.; Fong, D. G.; Foucher, M.; Fukui, H.; Frtjes, A.; Gagnon, P.; Gaidot, A.; Gary, J. W.; Gascon, J.; Gascon-Shotkin, S. M.; Geddes, N. I.; Geich-Gimbel, C.; Gentit, F. X.; Geralis, T.; Giacomelli, G.; Giacomelli, P.; Giacomelli, R.; Gibson, V.; Gibson, W. R.; Gingrich, D. M.; Goldberg, J.; Goodrick, M. J.; Gorn, W.; Grandi, C.; Gross, E.; Gruw, M.; Hajdu, C.; Hanson, G. G.; Hansroul, M.; Hapke, M.; Hargrove, C. K.; Hart, P. A.; Hartmann, C.; Hauschild, M.; Hawkes, C. M.; Hawkings, R.; Hemingway, R. J.; Herten, G.; Heuer, R. D.; Hildreth, M. D.; Hill, J. C.; Hillier, S. J.; Hilse, T.; Hoare, J.; Hobson, P. R.; Homer, R. J.; Honma, A. K.; Horvth, D.; Howard, R.; Hughes-Jones, R. E.; Hutchcroft, D. E.; Igo-Kemenes, P.; Imrie, D. C.; Ingram, M. R.; Jawahery, A.; Jeffreys, P. W.; Jeremie, H.; Jimack, M.; Joly, A.; Jones, C. R.; Jones, G.; Jones, M.; Jones, R. W. L.; Jost, U.; Jovanovic, P.; Junk, T. R.; Karlen, D.; Kawagoe, K.; Kawamoto, T.; Keeler, R. K.; Kellogg, R. G.; Kennedy, B. W.; King, B. J.; Kirk, J.; Kluth, S.; Kobayashi, T.; Kobel, M.; Koetke, D. S.; Kokott, T. P.; Komamiya, S.; Kowalewski, R.; Kress, T.; Krieger, P.; von Krogh, J.; Kyberd, P.; Lafferty, G. D.; Lafoux, H.; Lahmann, R.; Lai, W. P.; Lanske, D.; Lauber, J.; Lautenschlager, S. R.; Layter, J. G.; Lazic, D.; Lee, A. M.; Lefebvre, E.; Lellouch, D.; Letts, J.; Levinson, L.; Lewis, C.; Lloyd, S. L.; Loebinger, F. K.; Long, G. D.; Losty, M. J.; Ludwig, J.; Luig, A.; Malik, A.; Mannelli, M.; Marcellini, S.; Markus, C.; Martin, A. J.; Martin, J. P.; Martinez, G.; Mashimo, T.; Matthews, W.; Mttig, P.; McDonald, W. J.; McKenna, J.; McKigney, E. A.; McMahon, T. J.; McNab, A. I.; McPherson, R. A.; Meijers, F.; Menke, S.; Merritt, F. S.; Mes, H.; Meyer, J.; Michelini, A.; Mikenberg, G.; Miller, D. J.; Mir, R.; Mohr, W.; Montanari, A.; Mori, T.; Morii, M.; Mller, U.; Neal, H. A.; Nellen, B.; Nijjhar, B.; Nisius, R.; O'Neale, S. W.; Oakham, F. G.; Odorici, F.; Ogren, H. O.; Omori, T.; Oreglia, M. J.; Orito, S.; Plinks, J.; Pansart, J. P.; Psztor, G.; Pater, J. R.; Patrick, G. N.; Pearce, M. J.; Petzold, S.; Pfeifenschneider, P.; Pilcher, J. E.; Pinfold, J.; Plane, D. E.; Poffenberger, P.; Poli, B.; Posthaus, A.; Przysiezniak, H.; Rees, D. L.; Rigby, D.; Robins, S. A.; Rodning, N.; Roney, J. M.; Rooke, A.; Ros, E.; Rossi, A. M.; Rosvick, M.; Routenburg, P.; Rozen, Y.; Runge, K.; Runolfsson, O.; Ruppel, U.; Rust, D. R.; Rylko, R.; Sarkisyan, E. K. G.; Sasaki, M.; Sbarra, C.; Schaile, A. D.; Schaile, O.; Scharf, F.; Scharff-Hansen, P.; Schenk, P.; Schmitt, B.; Schmitt, S.; Schrder, M.; Schultz-Coulon, H. C.; Schulz, M.; Schtz, P.; Scott, W. G.; Shears, T. G.; Shen, B. C.; Shepherd-Themistocleous, C. H.; Sherwood, P.; Siroli, G. P.; Sittler, A.; Skillman, A.; Skuja, A.; Smith, A. M.; Smith, T. J.; Snow, G. A.; Sobie, R.; Sldner-Rembold, S.; Springer, R. W.; Sproston, M.; Stahl, A.; Starks, M.; Steiert, M.; Stephens, K.; Steuerer, J.; Stockhausen, B.; Strom, D.; Strumia, F.; Szymanski, P.; Tafirout, R.; Talbot, S. D.; Tanaka, S.; Taras, P.; Tarem, S.; Tecchio, M.; Thiergen, M.; Thomson, M. A.; von Trne, E.; Towers, S.; Tscheulin, M.; Tsukamoto, T.; Tsur, E.; Turcot, A. S.; Turner-Watson, M. F.; Utzat, P.; van Kooten, R.; Vasseur, G.; Verzocchi, M.; Vikas, P.; Vincter, M.; Vokurka, E. H.; Wckerle, F.; Wagner, A.; Ward, C. P.; Ward, D. R.; Ward, J. J.; Watkins, P. M.; Watson, A. T.; Watson, N. K.; Weber, P.; Wells, P. S.; Wermes, N.; White, J. S.; Wilkens, B.; Wilson, G. W.; Wilson, J. A.; Wlodek, T.; Wolf, G.; Wotton, S.; Wyatt, T. R.; Yamashita, S.; Yekutieli, G.; Zacek, V.

    1996-09-01

    A measurement of the ? lepton polarization and its forward-backward asymmetry at the Z0 resonance using the OPAL detector is described. The measurement is based on analyses of ?????, ???(K)??,tau to ebar ? _e ? _tau ,tau to ? bar ? _? ? _tau and ??a1 ? ? decays from a sample of 89075 e+e-? ? + ? - candidates corresponding to an integrated luminosity of 117 pb-1. Assuming that the ? lepton decays according to V-A theory, we measure the average ? polarization at ? s=MZ to be =(-13.00.90.9)% and the ? polarization forward-backward asymmetry to be A{pol/FB}=(-9.41.00.4)%, where the first error is statistical and the second systematic. These results are consistent with the hypothesis of lepton universality and, when combined, can be expressed as a measurement of sin2 ? {eff/lept}=0.23340.0012 within the context of the Standard Model.

  9. Greater Specificity for Cerebrospinal Fluid P-tau231 over P-tau181 in the Differentiation of Healthy Controls from Alzheimers Disease

    PubMed Central

    Spiegel, Jonathan; Pirraglia, Elizabeth; Osorio, Ricardo S.; Glodzik, Lidia; Li, Yi; Tsui, Wai; Saint Louis, Leslie A.; Randall, Catherine; Butler, Tracy; Xu, Jinfeng; Zinkowski, Raymond P.; Zetterberg, Henrik; Fortea, Juan; Fossati, Silvia; Wisniewski, Thomas; Davies, Peter; Blennow, Kaj; de Leon, Mony J.

    2015-01-01

    Cerebrospinal fluid (CSF) measures of phosphorylated-tau (P-tau) 231 and P-tau181 are two biomarkers for the identification of tau pathology as related to Alzheimers disease (AD). While both are pathologically validated, their relative diagnostic performances are not well known. This cross-sectional diagnostic study of 87 normal (NL) subjects and 28 AD subjects compared CSF P-tau231 with CSF P-tau181. Logistic regression modeling demonstrated that the P-tau231 was superior to the P-tau181 in the diagnostic classifications. At a fixed 85% sensitivity cutoff, the ROC analysis shows that P-tau231 has greater overall specificity than P-tau181. While both P-tau analytes demonstrated equivalent negative predictive accuracies, P-tau231 yielded significantly fewer false positives. Moreover, P-tau231, but not P-tau181, demonstrated sensitivity to the E4 genotype. A postmortem validation with 9 AD subjects confirmed the superiority of the CSF P-tau231 specificity. This study suggests that P-tau231 has the potential to improve the CSF tau biomarker diagnosis of AD. PMID:26444757

  10. Tau: The Center of a Signaling Nexus in Alzheimer's Disease

    PubMed Central

    Khan, Shahzad S.; Bloom, George S.

    2016-01-01

    Tau is a microtubule-associated protein whose misfolding, hyper-phosphorylation, loss of normal function and toxic gain of function are linked to several neurodegenerative disorders, including Alzheimer's disease (AD). This review discusses the role of tau in amyloid-β (Aβ) induced toxicity in AD. The consequences of tau dysfunction, starting from the axon and concluding at somadendritic compartments, will be highlighted. PMID:26903798

  11. MSUT2 is a determinant of susceptibility to tau neurotoxicity

    PubMed Central

    Guthrie, Chris R.; Greenup, Lynne; Leverenz, James B.; Kraemer, Brian C.

    2011-01-01

    Lesions containing abnormal aggregated tau protein are one of the diagnostic hallmarks of Alzheimer's disease (AD) and related tauopathy disorders. How aggregated tau leads to dementia remains enigmatic, although neuronal dysfunction and loss clearly contribute. We previously identified sut-2 as a gene required for tau neurotoxicity in a transgenic Caenorhabditis elegans model of tauopathy. Here, we further explore the role of sut-2 and show that overexpression of SUT-2 protein enhances tau-induced neuronal dysfunction, neurotoxicity and accumulation of insoluble tau. We also explore the relationship between sut-2 and its human homolog, mammalian SUT-2 (MSUT2) and find both proteins to be predominantly nuclear and localized to SC35-positive nuclear speckles. Using a cell culture model for the accumulation of pathological tau, we find that high tau levels lead to increased expression of MSUT2 protein. We analyzed MSUT2 protein in age-matched post-mortem brain samples from AD patients and observe a marked decrease in overall MSUT2 levels in the temporal lobe of AD patients. Analysis of post-mortem tissue from AD cases shows a clear reduction in neuronal MSUT2 levels in brain regions affected by tau pathology, but little change in regions lacking tau pathology. RNAi knockdown of MSUT2 in cultured human cells overexpressing tau causes a marked decrease in tau aggregation. Both cell culture and post-mortem tissue studies suggest that MSUT2 levels may influence neuronal vulnerability to tau toxicity and aggregation. Thus, neuroprotective strategies targeting MSUT2 may be of therapeutic interest for tauopathy disorders. PMID:21355046

  12. Tau-aggregation inhibitor therapy for Alzheimer's disease.

    PubMed

    Wischik, Claude M; Harrington, Charles R; Storey, John M D

    2014-04-15

    Many trials of drugs aimed at preventing or clearing ?-amyloid pathology have failed to demonstrate efficacy in recent years and further trials continue with drugs aimed at the same targets and mechanisms. The Alzheimer neurofibrillary tangle is composed of tau and the core of its constituent filaments are made of a truncated fragment from the repeat domain of tau. This truncated tau can catalyse the conversion of normal soluble tau into aggregated oligomeric and fibrillar tau which, in turn, can spread to neighbouring neurons. Tau aggregation is not a late-life process and onset of Braak stage 1 peaks in people in their late 40s or early 50s. Tau aggregation pathology at Braak stage 1 or beyond affects 50% of the population over the age of 45. The initiation of tau aggregation requires its binding to a non-specific substrate to expose a high affinity tau-tau binding domain and it is self-propagating thereafter. The initiating substrate complex is most likely formed as a consequence of a progressive loss of endosomal-lysosomal processing of neuronal proteins, particularly of membrane proteins from mitochondria. Mutations in the APP/presenilin membrane complex may simply add to the age-related endosomal-lysosomal processing failure, bringing forward, but not directly causing, the tau aggregation cascade in carriers. Methylthioninium chloride (MTC), the first identified tau aggregation inhibitor (TAI), offers an alternative to the amyloid approach. Phase 3 trials are underway with a novel stabilized reduced form of methylthioninium (LMTX) that has improved tolerability and absorption. PMID:24361915

  13. Prospects of constraining the Higgs boson's C P nature in the tau decay channel at the LHC

    NASA Astrophysics Data System (ADS)

    Berge, Stefan; Bernreuther, Werner; Kirchner, Sebastian

    2015-11-01

    We investigate how precisely the C P nature of the 125 GeV Higgs boson h , parametrized by a scalar-pseudoscalar Higgs mixing angle ??, can be determined in h ??-?+ decay with subsequent ? -lepton decays to charged prongs at the Large Hadron Collider (LHC). We combine two methods in order to define an observable ?CP * which is sensitive to ??: We use the ? -decay plane method for ????? and the impact parameter method for all other major ? decays. For estimating the precision with which ?? can be measured at the LHC (13 TeV) we take into account the ?-?+ background from Drell-Yan production and perform a Monte Carlo simulation of measurement uncertainties on the ?CP * signal and background distributions. We obtain that the mixing angle ?? can be determined with an uncertainty of ? ???1 5 (9) at the LHC with an integrated luminosity of 150 fb-1 (500 fb-1 ), and with ? ???4 with 3 ab-1 . Future measurements of ?? yield direct information on whether or not there is an extended Higgs-boson sector with Higgs-sector C P violation. We analyze this in the context of a number of two-Higgs-doublet extensions of the Standard Model, namely the so-called aligned model and conventional two-Higgs-doublet extensions with tree-level neutral flavor conservation.

  14. Tutorial guide to the tau lepton and close-mass lepton pairs

    SciTech Connect

    Perl, M.L.

    1988-10-01

    This is a tutorial guide to present knowledge of the tau lepton, to the tau decay mode puzzle, and to present searches for close-mass lepton pairs. The test is minimal; the emphasis is on figures, tables and literature references. It is based on a lecture given at the 1988 International School of Subnuclear Physics: The Super World III. 54 refs., 9 figs., 7 tabs.

  15. Accelerated neurodegeneration through chaperone-mediated oligomerization of tau.

    PubMed

    Blair, Laura J; Nordhues, Bryce A; Hill, Shannon E; Scaglione, K Matthew; O'Leary, John C; Fontaine, Sarah N; Breydo, Leonid; Zhang, Bo; Li, Pengfei; Wang, Li; Cotman, Carl; Paulson, Henry L; Muschol, Martin; Uversky, Vladimir N; Klengel, Torsten; Binder, Elisabeth B; Kayed, Rakez; Golde, Todd E; Berchtold, Nicole; Dickey, Chad A

    2013-10-01

    Aggregation of tau protein in the brain is associated with a class of neurodegenerative diseases known as tauopathies. FK506 binding protein 51 kDa (FKBP51, encoded by FKBP5) forms a mature chaperone complex with Hsp90 that prevents tau degradation. In this study, we have shown that tau levels are reduced throughout the brains of Fkbp5-/- mice. Recombinant FKBP51 and Hsp90 synergized to block tau clearance through the proteasome, resulting in tau oligomerization. Overexpression of FKBP51 in a tau transgenic mouse model revealed that FKBP51 preserved the species of tau that have been linked to Alzheimer's disease (AD) pathogenesis, blocked amyloid formation, and decreased tangle load in the brain. Alterations in tau turnover and aggregate structure corresponded with enhanced neurotoxicity in mice. In human brains, FKBP51 levels increased relative to age and AD, corresponding with demethylation of the regulatory regions in the FKBP5 gene. We also found that higher FKBP51 levels were associated with AD progression. Our data support a model in which age-associated increases in FKBP51 levels and its interaction with Hsp90 promote neurotoxic tau accumulation. Strategies aimed at attenuating FKBP51 levels or its interaction with Hsp90 have the potential to be therapeutically relevant for AD and other tauopathies. PMID:23999428

  16. Nitration of Tau Protein Is Linked to Neurodegeneration in Tauopathies

    PubMed Central

    Horiguchi, Takashi; Uryu, Kunihiro; Giasson, Benoit I.; Ischiropoulos, Harry; LightFoot, Richard; Bellmann, Christine; Richter-Landsberg, Christiane; Lee, Virginia M.-Y.; Trojanowski, John Q.

    2003-01-01

    Oxidative and nitrative injury is implicated in the pathogenesis of Alzheimers disease (AD) and Down syndrome (DS), but no direct evidence links this type of injury to the formation of neurofibrillary tau lesions. To address this, we generated a monoclonal antibody (mAb), n847, which recognizes nitrated tau and ?-synuclein. n847 detected nitrated tau in the insoluble fraction of AD, corticobasal degeneration (CBD), and Picks disease (PiD) brains by Western blots. Immunohistochemistry (IHC) showed that n847 labeled neurons in the hippocampus and neocortex of AD and DS brains. Double-label immunofluorescence with n847 and an anti-tau antibody revealed partial co-localization of tau and n847 positive tangles, while n847 immmunofluorescence and Thioflavin-S double-staining showed that a subset of n847-labeled neurons were Thioflavin-S-positive. In addition, immuno-electron microscopy revealed that tau-positive filaments in tangle-bearing neurons were also labeled by n847 and IHC of other tauopathies showed that some of glial and neuronal tau pathologies in CBD, progressive supranuclear palsy, PiD, and frontotemporal dementia with parkinsonism linked to chromosome 17 also were n847-positive. Finally, nitrated and Thioflavin-S-positive tau aggregates were generated in a oligodendrocytic cell line after treatment with peroxynitrite. Taken together, these findings imply that nitrative injury is directly linked to the formation of filamentous tau inclusions. PMID:12937143

  17. Nuclear Tau and Its Potential Role in Alzheimer's Disease.

    PubMed

    Bukar Maina, Mahmoud; Al-Hilaly, Youssra K; Serpell, Louise C

    2016-01-01

    Tau protein, found in both neuronal and non-neuronal cells, forms aggregates in neurons that constitutes one of the hallmarks of Alzheimer's disease (AD). For nearly four decades, research efforts have focused more on tau's role in physiology and pathology in the context of the microtubules, even though, for over three decades, tau has been localised in the nucleus and the nucleolus. Its nuclear and nucleolar localisation had stimulated many questions regarding its role in these compartments. Data from cell culture, mouse brain, and the human brain suggests that nuclear tau could be essential for genome defense against cellular distress. However, its nature of translocation to the nucleus, its nuclear conformation and interaction with the DNA and other nuclear proteins highly suggest it could play multiple roles in the nucleus. To find efficient tau-based therapies, there is a need to understand more about the functional relevance of the varied cellular distribution of tau, identify whether specific tau transcripts or isoforms could predict tau's localisation and function and how they are altered in diseases like AD. Here, we explore the cellular distribution of tau, its nuclear localisation and function and its possible involvement in neurodegeneration. PMID:26751496

  18. Tau approximation techniques for identification of coefficients in parabolic PDE

    NASA Technical Reports Server (NTRS)

    Banks, H. T.; Wade, J. G.

    1989-01-01

    A variant of the Tau method, called the weak Tau method, is developed on the basis of the weak form of the PDE for use in least-squares parameter estimation; also presented is a suitable abstract convergence framework. The emphasis is on the theoretical framework that allows treatment of the weak Tau method when it is applied to a wide class of inverse problems, including those for diffusion-advection equations, the Fokker-Planck model for population dynamics, and damped beam equations. Extensive numerical testing of the weak Tau method has demonstrated that it compares quite favorably with existing methods.

  19. Accelerated neurodegeneration through chaperone-mediated oligomerization of tau

    PubMed Central

    Blair, Laura J.; Nordhues, Bryce A.; Hill, Shannon E.; Scaglione, K. Matthew; OLeary, John C.; Fontaine, Sarah N.; Breydo, Leonid; Zhang, Bo; Li, Pengfei; Wang, Li; Cotman, Carl; Paulson, Henry L.; Muschol, Martin; Uversky, Vladimir N.; Klengel, Torsten; Binder, Elisabeth B.; Kayed, Rakez; Golde, Todd E.; Berchtold, Nicole; Dickey, Chad A.

    2013-01-01

    Aggregation of tau protein in the brain is associated with a class of neurodegenerative diseases known as tauopathies. FK506 binding protein 51 kDa (FKBP51, encoded by FKBP5) forms a mature chaperone complex with Hsp90 that prevents tau degradation. In this study, we have shown that tau levels are reduced throughout the brains of Fkbp5/ mice. Recombinant FKBP51 and Hsp90 synergized to block tau clearance through the proteasome, resulting in tau oligomerization. Overexpression of FKBP51 in a tau transgenic mouse model revealed that FKBP51 preserved the species of tau that have been linked to Alzheimers disease (AD) pathogenesis, blocked amyloid formation, and decreased tangle load in the brain. Alterations in tau turnover and aggregate structure corresponded with enhanced neurotoxicity in mice. In human brains, FKBP51 levels increased relative to age and AD, corresponding with demethylation of the regulatory regions in the FKBP5 gene. We also found that higher FKBP51 levels were associated with AD progression. Our data support a model in which age-associated increases in FKBP51 levels and its interaction with Hsp90 promote neurotoxic tau accumulation. Strategies aimed at attenuating FKBP51 levels or its interaction with Hsp90 have the potential to be therapeutically relevant for AD and other tauopathies. PMID:23999428

  20. Somatodendritic localization and hyperphosphorylation of tau protein in transgenic mice expressing the longest human brain tau isoform.

    PubMed Central

    Gtz, J; Probst, A; Spillantini, M G; Schfer, T; Jakes, R; Brki, K; Goedert, M

    1995-01-01

    Microtubule-associated protein tau is the major constituent of the paired helical filament, the main fibrous component of the neurofibrillary lesions of Alzheimer's disease. Tau is an axonal phosphoprotein in normal adult brain. In Alzheimer's disease brain tau is hyperphosphorylated and is found not only in axons, but also in cell bodies and dendrites of affected nerve cells. We report the production and analysis of transgenic mice that express the longest human brain tau isoform under the control of the human Thy-1 promoter. As in Alzheimer's disease, transgenic human tau protein was present in nerve cell bodies, axons and dendrites; moreover, it was phosphorylated at sites that are hyperphosphorylated in paired helical filaments. We conclude that transgenic human tau protein showed pre-tangle changes similar to those that precede the full neurofibrillary pathology in Alzheimer's disease. Images PMID:7729409

  1. Measurement of cross-section (p anti-p --> Z0) x BF (Z0 --> tau anti-tau) at s**(1/2) = 1.96-TeV using the D0 detector at the Tevatron

    SciTech Connect

    Duensing, Silke

    2004-04-01

    In this thesis the first measurement of {sigma}(p{bar p}) {yields} Z{sup 0} {yields} {tau}{bar {tau}} with the D0 detector at the Tevatron is presented. The tau pair candidates are recorded by the D0 detector using p{bar p} interactions at a center-of-mass energy of 1.96 TeV. Events in which one tau decays into a muon and the other tau final state is hadronic with one charged particle are selected for this analysis. The selection criteria for the hadronic tau decay are based on the tau final state, hence for two channels of one-prong taus: single charged pion ({tau}{sub {pi}}) and rho decays ({tau}{sub {rho}}). The selection is based on simple cuts on a number of discriminating variables and the cut values have been optimized for the best cross section measurement. Of hadronic tau candidates that have been reconstructed as {tau}{sub {pi}} candidates, 0.801 {+-} 0.017 {+-} 0.066 pass the selection cut; in the case of {tau}{sub {rho}} taus, the selection efficiency is 0.676 {+-} 0.009 {+-} 0.009. Of all QCD jets that are reconstructed as hadronic tau candidates, 0.0093 {+-} 0.0002 pass the {tau}{sub {pi}} selection cuts and 0.0122 {+-} 0.0002 the {tau}{sub {rho}} cuts. The cross section has been measured to be 274 {+-} 121 {+-} 40 {+-} 27 pb in the {mu}{tau}{sub {pi}} channel and 273 {+-} 40{sub -23}{sup +18} {+-} 27 pb in the {mu}{tau}{sub {rho}} channel, resulting in a combined measurement of {sigma}(p{bar p} {yields} Z{sup 0} {yields} {tau}{bar {tau}}) = 273 {+-} 38{sub -23}{sup +19} {+-} 27 pb which agrees with the SM prediction within errors. The errors are dominated by the statistical error as only the first data taken with the D0 detector in Run II was used. Due to the small set of tau candidates, the calorimeter energy scale could not yet be determined using data and this uncertainty is the largest systematic effect on the measurement. Another large contribution arises from the uncertainty of 10% on the luminosity measurement. This is expected to decrease significantly in the future. It was demonstrated that the currently available tools are sufficient to use tau leptons in the measurement of a SM process. This opens the door to the use of hadronic tau decays in the search for new particles, like SUSY particles, that decay preferentially to tau leptons in a number of models or the Higgs boson of either the SM or extended model. Doing physics at the Tevatron as the accelerator at the current energy frontier is our current best hope to find the yet elusive Higgs boson and will allow to either find proof of physics beyond the Standard Model or tighten the constraints on these models.

  2. Upper limit on the diffuse flux of UHE tau neutrinos from the Pierre Auger Observatory

    SciTech Connect

    Collaboration, The Pierre Auger

    2007-12-01

    The surface detector array of the Pierre Auger Observatory is sensitive to Earth-skimming tau-neutrinos {nu}{sub {tau}} that interact in the Earth's crust. Tau leptons from {tau}{sub {tau}} charged-current interactions can emerge and decay in the atmosphere to produce a nearly horizontal shower with a significant electromagnetic component. The data collected between 1 January 2004 and 31 August 2007 is used to place an upper limit on the diffuse flux of {nu}{sub {tau}} at EeV energies. Assuming an E{sub {nu}}{sup -2} differential energy spectrum the limit set at 90 % C.L. is E{sub {nu}}{sup 2} dN{sub {nu}{sub {tau}}}/dE{sub {nu}} < 1.3 x 10{sup -7} GeV cm{sup -2} s{sup -1} sr{sup -1} in the energy range 2 x 10{sup 17} eV < E{sub {nu}} < 2 x 10{sup 19} eV.

  3. Discovering the Higgs bosons of minimal supersymmetry with tau leptons and a bottom quark

    SciTech Connect

    Kao, Chung; Dicus, Duane A.; Malhotra, Rahul; Wang Yili

    2008-05-01

    We investigate the prospects for the discovery at the CERN Large Hadron Collider or at the Fermilab Tevatron of neutral Higgs bosons through the channel where the Higgs are produced together with a single bottom quark and the Higgs decays into a pair of tau leptons, bg{yields}b{phi}{sup 0}{yields}b{tau}{sup +}{tau}{sup -}, {phi}{sup 0}=h{sup 0}, H{sup 0}, A{sup 0}. We work within the framework of the minimal supersymmetric model. The dominant physics background from the production of b{tau}{sup +}{tau}{sup -}, j{tau}{sup +}{tau}{sup -} (j=g,u,d,s,c), bbW{sup +}W{sup -}, W+2j, and Wbj is calculated with realistic acceptance cuts and efficiencies. Promising results are found for the CP-odd pseudoscalar (A{sup 0}) and the heavier CP-even scalar (H{sup 0}) Higgs bosons with masses up to one TeV.

  4. Intermediate overtone oscillations of Tau CYG

    NASA Astrophysics Data System (ADS)

    Mkritichian, D. E.; Fedotov, Y. T.; Romanov, Y. S.

    1995-01-01

    According to GCVS (Kholopov et al, 1985) classification Tau Cyg (V=3.70m, F0 IV) is a Delta Scuti type pulsating variable star. However, as is seen from history of its investigations (Paraskevopulos, 1921; Henroteau, 1922; Abt, 1961; Pant et al., 1968; Breger, 1969; Millis, 1969; Fesen, 1973; Bartolini and Dapergolas, 1980; Andrievski and Garbusov, 1987), the conclusions made by different investigators on pulsational activity are ambiguous, and the question on the variability character and possible periodicities remains unsolved for the present, in spite of the stars brightness and the facility for its observations.

  5. Search for the standard model Higgs boson in tau final states.

    PubMed

    Abazov, V M; Abbott, B; Abolins, M; Acharya, B S; Adams, M; Adams, T; Aguilo, E; Ahsan, M; Alexeev, G D; Alkhazov, G; Alton, A; Alverson, G; Alves, G A; Ancu, L S; Andeen, T; Anzelc, M S; Aoki, M; Arnoud, Y; Arov, M; Arthaud, M; Askew, A; Asman, B; Atramentov, O; Avila, C; Backusmayes, J; Badaud, F; Bagby, L; Baldin, B; Bandurin, D V; Banerjee, S; Barberis, E; Barfuss, A-F; Bargassa, P; Baringer, P; Barreto, J; Bartlett, J F; Bassler, U; Bauer, D; Beale, S; Bean, A; Begalli, M; Begel, M; Belanger-Champagne, C; Bellantoni, L; Bellavance, A; Benitez, J A; Beri, S B; Bernardi, G; Bernhard, R; Bertram, I; Besançon, M; Beuselinck, R; Bezzubov, V A; Bhat, P C; Bhatnagar, V; Blazey, G; Blessing, S; Bloom, K; Boehnlein, A; Boline, D; Bolton, T A; Boos, E E; Borissov, G; Bose, T; Brandt, A; Brock, R; Brooijmans, G; Bross, A; Brown, D; Bu, X B; Buchholz, D; Buehler, M; Buescher, V; Bunichev, V; Burdin, S; Burnett, T H; Buszello, C P; Calfayan, P; Calpas, B; Calvet, S; Cammin, J; Carrasco-Lizarraga, M A; Carrera, E; Carvalho, W; Casey, B C K; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K M; Chandra, A; Cheu, E; Cho, D K; Choi, S; Choudhary, B; Christoudias, T; Cihangir, S; Claes, D; Clutter, J; Cooke, M; Cooper, W E; Corcoran, M; Couderc, F; Cousinou, M-C; Crépé-Renaudin, S; Cuplov, V; Cutts, D; Cwiok, M; Das, A; Davies, G; De, K; de Jong, S J; De La Cruz-Burelo, E; DeVaughan, K; Déliot, F; Demarteau, M; Demina, R; Denisov, D; Denisov, S P; Desai, S; Diehl, H T; Diesburg, M; Dominguez, A; Dorland, T; Dubey, A; Dudko, L V; Duflot, L; Duggan, D; Duperrin, A; Dutt, S; Dyshkant, A; Eads, M; Edmunds, D; Ellison, J; Elvira, V D; Enari, Y; Eno, S; Ermolov, P; Escalier, M; Evans, H; Evdokimov, A; Evdokimov, V N; Facini, G; Ferapontov, A V; Ferbel, T; Fiedler, F; Filthaut, F; Fisher, W; Fisk, H E; Fortner, M; Fox, H; Fu, S; Fuess, S; Gadfort, T; Galea, C F; Garcia-Bellido, A; Gavrilov, V; Gay, P; Geist, W; Geng, W; Gerber, C E; Gershtein, Y; Gillberg, D; Ginther, G; Gómez, B; Goussiou, A; Grannis, P D; Greder, S; Greenlee, H; Greenwood, Z D; Gregores, E M; Grenier, G; Gris, Ph; Grivaz, J-F; Grohsjean, A; Grünendahl, S; Grünewald, M W; Guo, F; Guo, J; Gutierrez, G; Gutierrez, P; Haas, A; Hadley, N J; Haefner, P; Hagopian, S; Haley, J; Hall, I; Hall, R E; Han, L; Harder, K; Harel, A; Hauptman, J M; Hays, J; Hebbeker, T; Hedin, D; Hegeman, J G; Heinson, A P; Heintz, U; Hensel, C; Heredia-De La Cruz, I; Herner, K; Hesketh, G; Hildreth, M D; Hirosky, R; Hoang, T; Hobbs, J D; Hoeneisen, B; Hohlfeld, M; Hossain, S; Houben, P; Hu, Y; Hubacek, Z; Huske, N; Hynek, V; Iashvili, I; Illingworth, R; Ito, A S; Jabeen, S; Jaffré, M; Jain, S; Jakobs, K; Jamin, D; Jarvis, C; Jesik, R; Johns, K; Johnson, C; Johnson, M; Johnston, D; Jonckheere, A; Jonsson, P; Juste, A; Kajfasz, E; Karmanov, D; Kasper, P A; Katsanos, I; Kaushik, V; Kehoe, R; Kermiche, S; Khalatyan, N; Khanov, A; Kharchilava, A; Kharzheev, Y N; Khatidze, D; Kim, T J; Kirby, M H; Kirsch, M; Klima, B; Kohli, J M; Konrath, J-P; Kozelov, A V; Kraus, J; Kuhl, T; Kumar, A; Kupco, A; Kurca, T; Kuzmin, V A; Kvita, J; Lacroix, F; Lam, D; Lammers, S; Landsberg, G; Lebrun, P; Lee, W M; Leflat, A; Lellouch, J; Li, J; Li, L; Li, Q Z; Lietti, S M; Lim, J K; Lincoln, D; Linnemann, J; Lipaev, V V; Lipton, R; Liu, Y; Liu, Z; Lobodenko, A; Lokajicek, M; Love, P; Lubatti, H J; Luna-Garcia, R; Lyon, A L; Maciel, A K A; Mackin, D; Mättig, P; Magerkurth, A; Mal, P K; Malbouisson, H B; Malik, S; Malyshev, V L; Maravin, Y; Martin, B; McCarthy, R; McGivern, C L; Meijer, M M; Melnitchouk, A; Mendoza, L; Menezes, D; Mercadante, P G; Merkin, M; Merritt, K W; Meyer, A; Meyer, J; Mitrevski, J; Mommsen, R K; Mondal, N K; Moore, R W; Moulik, T; Muanza, G S; Mulhearn, M; Mundal, O; Mundim, L; Nagy, E; Naimuddin, M; Narain, M; Neal, H A; Negret, J P; Neustroev, P; Nilsen, H; Nogima, H; Novaes, S F; Nunnemann, T; Obrant, G; Ochando, C; Onoprienko, D; Orduna, J; Oshima, N; Osman, N; Osta, J; Otec, R; Otero Y Garzón, G J; Owen, M; Padilla, M; Padley, P; Pangilinan, M; Parashar, N; Park, S-J; Park, S K; Parsons, J; Partridge, R; Parua, N; Patwa, A; Pawloski, G; Penning, B; Perfilov, M; Peters, K; Peters, Y; Pétroff, P; Piegaia, R; Piper, J; Pleier, M-A; Podesta-Lerma, P L M; Podstavkov, V M; Pogorelov, Y; Pol, M-E; Polozov, P; Popov, A V; Potter, C; Prado da Silva, W L; Protopopescu, S; Qian, J; Quadt, A; Quinn, B; Rakitine, A; Rangel, M S; Ranjan, K; Ratoff, P N; Renkel, P; Rich, P; Rijssenbeek, M; Ripp-Baudot, I; Rizatdinova, F; Robinson, S; Rodrigues, R F; Rominsky, M; Royon, C; Rubinov, P; Ruchti, R; Safronov, G; Sajot, G; Sánchez-Hernández, A; Sanders, M P; Sanghi, B; Savage, G; Sawyer, L; Scanlon, T; Schaile, D; Schamberger, R D; Scheglov, Y; Schellman, H; Schliephake, T; Schlobohm, S; Schwanenberger, C; Schwienhorst, R; Sekaric, J; Severini, H; Shabalina, E; Shamim, M; Shary, V; Shchukin, A A; Shivpuri, R K; Siccardi, V; Simak, V; Sirotenko, V; Skubic, P; Slattery, P; Smirnov, D; Snow, G R; Snow, J; Snyder, S; Söldner-Rembold, S; Sonnenschein, L; Sopczak, A; Sosebee, M; Soustruznik, K; Spurlock, B; Stark, J; Stolin, V; Stoyanova, D A; Strandberg, J; Strandberg, S; Strang, M A; Strauss, E; Strauss, M; Ströhmer, R; Strom, D; Stutte, L; Sumowidagdo, S; Svoisky, P; Takahashi, M; Tanasijczuk, A; Taylor, W; Tiller, B; Tissandier, F; Titov, M; Tokmenin, V V; Torchiani, I; Tsybychev, D; Tuchming, B; Tully, C; Tuts, P M; Unalan, R; Uvarov, L; Uvarov, S; Uzunyan, S; Vachon, B; van den Berg, P J; Van Kooten, R; van Leeuwen, W M; Varelas, N; Varnes, E W; Vasilyev, I A; Verdier, P; Vertogradov, L S; Verzocchi, M; Vilanova, D; Vint, P; Vokac, P; Voutilainen, M; Wagner, R; Wahl, H D; Wang, M H L S; Warchol, J; Watts, G; Wayne, M; Weber, G; Weber, M; Welty-Rieger, L; Wenger, A; Wetstein, M; White, A; Wicke, D; Williams, M R J; Wilson, G W; Wimpenny, S J; Wobisch, M; Wood, D R; Wyatt, T R; Xie, Y; Xu, C; Yacoob, S; Yamada, R; Yang, W-C; Yasuda, T; Yatsunenko, Y A; Ye, Z; Yin, H; Yip, K; Yoo, H D; Youn, S W; Yu, J; Zeitnitz, C; Zelitch, S; Zhao, T; Zhou, B; Zhu, J; Zielinski, M; Zieminska, D; Zivkovic, L; Zutshi, V; Zverev, E G

    2009-06-26

    We present a search for the standard model Higgs boson using hadronically decaying tau leptons, in 1 fb(-1) of data collected with the D0 detector at the Fermilab Tevatron pp collider. We select two final states: tau+/- plus missing transverse energy and b jets, and tau+ tau- plus jets. These final states are sensitive to a combination of associated W/Z boson plus Higgs boson, vector boson fusion, and gluon-gluon fusion production processes. The observed ratio of the combined limit on the Higgs production cross section at the 95% C.L. to the standard model expectation is 29 for a Higgs boson mass of 115 GeV. PMID:19659068

  6. Biochemistry and Cell Biology of Tau Protein in Neurofibrillary Degeneration

    PubMed Central

    Mandelkow, Eva-Maria; Mandelkow, Eckhard

    2012-01-01

    Tau represents the subunit protein of one of the major hallmarks of Alzheimer disease (AD), the neurofibrillary tangles, and is therefore of major interest as an indicator of disease mechanisms. Many of the unusual properties of Tau can be explained by its nature as a natively unfolded protein. Examples are the large number of structural conformations and biochemical modifications (phosphorylation, proteolysis, glycosylation, and others), the multitude of interaction partners (mainly microtubules, but also other cytoskeletal proteins, kinases, and phosphatases, motor proteins, chaperones, and membrane proteins). The pathological aggregation of Tau is counterintuitive, given its high solubility, but can be rationalized by short hydrophobic motifs forming β structures. The aggregation of Tau is toxic in cell and animal models, but can be reversed by suppressing expression or by aggregation inhibitors. This review summarizes some of the structural, biochemical, and cell biological properties of Tau and Tau fibers. Further aspects of Tau as a diagnostic marker and therapeutic target, its involvement in other Tau-based diseases, and its histopathology are covered by other chapters in this volume. PMID:22762014

  7. Pseudophosphorylation of tau protein directly modulates its aggregation kinetics

    PubMed Central

    Chang, Edward; Kim, Sohee; Schafer, Kelsey N.; Kuret, Jeff

    2010-01-01

    Hyperphosphorylation of tau protein is associated with neurofibrillary lesion formation in Alzheimer’s disease and other tauopathic neurodegenerative diseases. It fosters lesion formation by increasing the concentration of free tau available for aggregation and by directly modulating the tau aggregation reaction. To clarify how negative charge incorporation into tau directly affects aggregation behavior, the fibrillization of pseudophosphorylation mutant T212E prepared in a full-length four-repeat tau background was examined in vitro as a function of time and submicromolar tau concentrations using electron microscopy assay methods. Kinetic constants for nucleation and extension phases of aggregation were then estimated by direct measurement and mathematical simulation. Kinetic analysis revealed that pseudophosphorylation increased tau aggregation rate by increasing the rate of filament nucleation. In addition, it increased aggregation propensity by stabilizing mature filaments against disaggregation. The data suggest that incorporation of negative charge into the T212 site can directly promote tau filament formation at multiple steps in the aggregation pathway. PMID:20974297

  8. Methylglyoxal induces tau hyperphosphorylation via promoting AGEs formation.

    PubMed

    Li, Xiao-Hong; Xie, Jia-Zhao; Jiang, Xia; Lv, Bing-Ling; Cheng, Xiang-Shu; Du, Lai-Ling; Zhang, Jia-Yu; Wang, Jian-Zhi; Zhou, Xin-Wen

    2012-12-01

    The hyperphosphorylated tau is a major protein component of neurofibrillary tangle, which is one of hallmarks of Alzheimer's disease (AD). While the level of methylglyoxal (MG) is significantly increased in the AD brains, the role of MG in tau phosphorylation is still not reported. Here, we found that MG could induce tau hyperphosphorylation at multiple AD-related sites in neuroblastoma 2a cells under maintaining normal cell viability. MG treatment increased the level of advanced glycation end products (AGEs) and the receptor of AGEs (RAGE). Glycogen synthesis kinase-3β (GSK-3β) and p38 MAPK were activated, whereas the level and activity of JNK, Erk1/2, cdk5, and PP2A were not altered after MG treatment. Simultaneous inhibition of GSK-3β or p38 attenuated the MG-induced tau hyperphosphorylation. Aminoguanidine, a blocker of AGEs formation, could effectively reverse the MG-induced tau hyperphosphorylation. These data suggest that MG induces AD-like tau hyperphosphorylation through AGEs formation involving RAGE up-regulation and GSK-3β activation and p38 activation is also partially involved in MG-induced tau hyperphosphorylation. Thus, targeting MG may be a promising therapeutic strategy to prevent AD-like tau hyperphosphorylation. PMID:22798221

  9. Tau-adaptivity for nonsmooth processes in heterogeneous media

    NASA Astrophysics Data System (ADS)

    Brown, J.; Adams, M.; Knepley, M.

    2014-12-01

    We propose a form of adaptivity based on FAS multigrid and related to the "frozen ?tau technique proposed by Achi Brandt, allowing fine grid work to be avoided in regions with nearly-linear behavior, despite arbitrarily rough coefficients. We investigate indicators for reuse of ?tau, practicality of dynamic load balancing, and experiment with localized plastic yielding in lithosphere dynamics.

  10. Tau and neurodegenerative disease: the story so far.

    PubMed

    Iqbal, Khalid; Liu, Fei; Gong, Cheng-Xin

    2016-01-01

    In 1975, tau protein was isolated as a microtubule-associated factor from the porcine brain. In the previous year, a paired helical filament (PHF) protein had been identified in neurofibrillary tangles in the brains of individuals with Alzheimer disease (AD), but it was not until 1986 that the PHF protein and tau were discovered to be one and the same. In the AD brain, tau was found to be abnormally hyperphosphorylated, and it inhibited rather than promoted in vitro microtubule assembly. Almost 80 disease-causing exonic missense and intronic silent mutations in the tau gene have been found in familial cases of frontotemporal dementia but, to date, no such mutation has been found in AD. The first phase I clinical trial of an active tau immunization vaccine in patients with AD was recently completed. Assays for tau levels in cerebrospinal fluid and plasma are now available, and tau radiotracers for PET are under development. In this article, we provide an overview of the pivotal discoveries in the tau research field over the past 40 years. We also review the current status of the field, including disease mechanisms and therapeutic approaches. PMID:26635213

  11. Identification of nuclear. tau. isoforms in human neuroblastoma cells

    SciTech Connect

    Loomis, P.A.; Howard, T.H.; Castleberry, R.P.; Binder, L.I. )

    1990-11-01

    The {tau} proteins have been reported only in association with microtubules and with ribosomes in situ, in the normal central nervous system. In addition, {tau} has been shown to be an integral component of paired helical filaments, the principal constituent of the neurofibrillary tangles found in brains of patients with Alzheimer's disease and of most aged individuals with Down syndrome (trisomy 21). The authors report here the localization of the well-characterized Tau-1 monoclonal antibody to the nucleolar organizer regions of the acrocentric chromosomes and to their interphase counterpart, the fibrillar component of the nucleolus, in human neuroblastoma cells. Similar localization to the nucleolar organizer regions was also observed in other human cell lines and in one monkey kidney cell line but was not seen in non-primate species. Immunochemically, they further demonstrated the existence of the entire {tau} molecule in the isolated nuclei of neuroblastoma cells. Nuclear {tau} proteins, like the {tau} proteins of the paired helical filaments, cannot be extracted in standard SDS-containing electrophoresis sample buffer but require pretreatment with formic acid prior to immunoblot analysis. This work indicates that {tau} may function in processes not directly associated with microtubules and that highly insoluble complexes of {tau} may also play a role in normal cellular physiology.

  12. Comparative biochemistry of tau in progressive supranuclear palsy, corticobasal degeneration, FTDP-17 and Pick's disease.

    PubMed

    Buée, L; Delacourte, A

    1999-10-01

    Neurodegenerative disorders referred to as tauopathies have cellular hyperphosphorylated tau protein aggregates in the absence of amyloid deposits. Comparative biochemistry of tau aggregates shows that they differ in both phosphorylation and content of tau isoforms. The six tau isoforms found in human brain contain either three (3R) or four microtubule-binding domains (4R). In Alzheimer's disease, all six tau isoforms are abnormally phosphorylated and aggregate into paired helical filaments. They are detected by immunoblotting as a major tau triplet (tau55, 64 and 69). In corticobasal degeneration and progressive supranuclear palsy, only 4R-tau isoforms aggregate into twisted and straight filaments respectively. They appear as a major tau doublet (tau64 and 69). Finally, in Pick's disease, only 3R-tau isoforms aggregate into random coiled filaments. They are characterized by another major tau doublet (tau55 and 64). These differences in tau isoforms may be related to either the degeneration of particular cell populations in a given disorder or aberrant cell trafficking of particular tau isoforms. Finally, recent findings provide a direct link between a genetic defect in tau and its abnormal aggregation into filaments in fronto-temporal dementia with Parkinsonism linked to chromosome 17, demonstrating that tau aggregation is sufficient for nerve cell degeneration. Thus, tau mutations and polymorphisms may also be instrumental in many neurodegenerative disorders. PMID:10517507

  13. Tau co-organizes dynamic microtubule and actin networks

    PubMed Central

    Elie, Aurliane; Prezel, Elea; Gurin, Christophe; Denarier, Eric; Ramirez-Rios, Sacnicte; Serre, Laurence; Andrieux, Annie; Fourest-Lieuvin, Anne; Blanchoin, Laurent; Arnal, Isabelle

    2015-01-01

    The crosstalk between microtubules and actin is essential for cellular functions. However, mechanisms underlying the microtubule-actin organization by cross-linkers remain largely unexplored. Here, we report that tau, a neuronal microtubule-associated protein, binds to microtubules and actin simultaneously, promoting in vitro co-organization and coupled growth of both networks. By developing an original assay to visualize concomitant microtubule and actin assembly, we show that tau can induce guided polymerization of actin filaments along microtubule tracks and growth of single microtubules along actin filament bundles. Importantly, tau mediates microtubule-actin co-alignment without changing polymer growth properties. Mutagenesis studies further reveal that at least two of the four tau repeated motifs, primarily identified as tubulin-binding sites, are required to connect microtubules and actin. Tau thus represents a molecular linker between microtubule and actin networks, enabling a coordination of the two cytoskeletons that might be essential in various neuronal contexts. PMID:25944224

  14. The Excitotoxin Quinolinic Acid Induces Tau Phosphorylation in Human Neurons

    PubMed Central

    Ting, Kaka; Cullen, Karen M.; Braidy, Nady; Brew, Bruce J.

    2009-01-01

    Some of the tryptophan catabolites produced through the kynurenine pathway (KP), and more particularly the excitotoxin quinolinic acid (QA), are likely to play a role in the pathogenesis of Alzheimer's disease (AD). We have previously shown that the KP is over activated in AD brain and that QA accumulates in amyloid plaques and within dystrophic neurons. We hypothesized that QA in pathophysiological concentrations affects tau phosphorylation. Using immunohistochemistry, we found that QA is co-localized with hyperphosphorylated tau (HPT) within cortical neurons in AD brain. We then investigated in vitro the effects of QA at various pathophysiological concentrations on tau phosphorylation in primary cultures of human neurons. Using western blot, we found that QA treatment increased the phosphorylation of tau at serine 199/202, threonine 231 and serine 396/404 in a dose dependent manner. Increased accumulation of phosphorylated tau was also confirmed by immunocytochemistry. This increase in tau phosphorylation was paralleled by a substantial decrease in the total protein phosphatase activity. A substantial decrease in PP2A expression and modest decrease in PP1 expression were observed in neuronal cultures treated with QA. These data clearly demonstrate that QA can induce tau phosphorylation at residues present in the PHF in the AD brain. To induce tau phosphorylation, QA appears to act through NMDA receptor activation similar to other agonists, glutamate and NMDA. The QA effect was abrogated by the NMDA receptor antagonist memantine. Using PCR arrays, we found that QA significantly induces 10 genes in human neurons all known to be associated with AD pathology. Of these 10 genes, 6 belong to pathways involved in tau phosphorylation and 4 of them in neuroprotection. Altogether these results indicate a likely role of QA in the AD pathology through promotion of tau phosphorylation. Understanding the mechanism of the neurotoxic effects of QA is essential in developing novel therapeutic strategies for AD. PMID:19623258

  15. Mechanisms of tau and Aβ-induced excitotoxicity.

    PubMed

    Pallo, Susanne P; DiMaio, John; Cook, Alexis; Nilsson, Bradley; Johnson, Gail V W

    2016-03-01

    Excitotoxicity was originally postulated to be a late stage side effect of Alzheimer׳s disease (AD)-related neurodegeneration, however more recent studies indicate that it may occur early in AD and contribute to the neurodegenerative process. Tau and amyloid beta (Aβ), the main components of neurofibrillary tangles (NFTs) and amyloid plaques, have been implicated in cooperatively and independently facilitating excitotoxicity. Our study investigated the roles of tau and Aβ in AD-related excitotoxicity. In vivo studies showed that tau knockout (tau(-/-)) mice were significantly protected from seizures and hippocampal superoxide production induced with the glutamate analog, kainic acid (KA). We hypothesized that tau accomplished this by facilitating KA-induced Ca(2+) influx into neurons, however lentiviral tau knockdown failed to ameliorate KA-induced Ca(2+) influx into primary rat cortical neurons. We further investigated if tau cooperated with Aβ to facilitate KA-induced Ca(2+) influx. While Aβ biphasically modulated the KA-induced Cacyt(2+) responses, tau knockdown continued to have no effect. Therefore, tau facilitates KA-induced seizures and superoxide production in a manner that does not involve facilitation of Ca(2+) influx through KA receptors (KAR). On the other hand, acute pretreatment with Aβ (10min) enhanced KA-induced Ca(2+) influx, while chronic Aβ (24h) significantly reduced it, regardless of tau knockdown. Given previously published connections between Aβ, group 1 metabotropic glutamate receptors (mGluRs), and KAR regulation, we hypothesized that Aβ modulates KAR via a G-protein coupled receptor pathway mediated by group 1mGluRs. We found that Aβ did not activate group 1mGluRs and inhibition of these receptors did not reverse Aβ modulation of KA-induced Ca(2+) influx. Therefore, Aβ biphasically regulates KAR via a mechanism that does not involve group 1mGluR activation. PMID:26731336

  16. Search for heavy neutrinos mixing with tau neutrinos

    NASA Astrophysics Data System (ADS)

    NOMAD Collaboration; Astier, P.; Autiero, D.; Baldisseri, A.; Baldo-Ceolin, M.; Banner, M.; Bassompierre, G.; Benslama, K.; Besson, N.; Bird, I.; Blumenfeld, B.; Bobisut, F.; Bouchez, J.; Boyd, S.; Bueno, A.; Bunyatov, S.; Camilleri, L.; Cardini, A.; Cattaneo, P. W.; Cavasinni, V.; Cervera-Villanueva, A.; Collazuol, G.; Conforto, G.; Conta, C.; Contalbrigo, M.; Cousins, R.; Daniels, D.; Degaudenzi, H.; Del Prete, T.; De Santo, A.; Dignan, T.; Di Lella, L.; do Couto e Silva, E.; Donnelly, I. J.; Dumarchez, J.; Ellis, M.; Fazio, T.; Feldman, G. J.; Ferrari, R.; Ferrre, D.; Flaminio, V.; Fraternali, M.; Gaillard, J.-M.; Gangler, E.; Geiser, A.; Geppert, D.; Gibin, D.; Gninenko, S. N.; Godley, A.; Gonzalez-Garcia, M. C.; Gomez-Cadenas, J.-J.; Gosset, J.; Gling, C.; Gouanre, M.; Grant, A.; Graziani, G.; Guglielmi, A.; Hagner, C.; Hernando, J.; Hubbard, D.; Hurst, P.; Hyett, N.; Iacopini, E.; Joseph, C.; Juget, F.; Kirsanov, M. M.; Klimov, O.; Kokkonen, J.; Kovzelev, A. V.; Krasnikov, N. V.; Krasnoperov, A.; Lacaprara, S.; Lachaud, C.; Laki?, B.; Lanza, A.; La Rotonda, L.; Laveder, M.; Letessier-Selvon, A.; Levy, J.-M.; Linssen, L.; Ljubi?i?, A.; Long, J.; Lupi, A.; Marchionni, A.; Martelli, F.; Mchain, X.; Mendiburu, J.-P.; Meyer, J.-P.; Mezzetto, M.; Mishra, S. R.; Moorhead, G. F.; Naumov, D.; Ndlec, P.; Nefedov, Y.; Nguyen-Mau, C.; Orestano, D.; Pastore, F.; Peak, L. S.; Pennacchio, E.; Pessard, H.; Petti, R.; Placci, A.; Polesello, G.; Pollmann, D.; Polyarush, A.; Popov, B.; Poulsen, C.; Rathouit, P.; Rico, J.; Roda, C.; Rubbia, A.; Salvatore, F.; Schahmaneche, K.; Schmidt, B.; Segneri, G.; Sevior, M.; Soler, F. J. P.; Sozzi, G.; Steele, D.; Stiegler, U.; Stip?evi?, M.; Stolarczyk, T.; Tareb-Reyes, M.; Taylor, G. N.; Tereshchenko, V.; Toropin, A. N.; Touchard, A.-M.; Tovey, S. N.; Tran, M.-T.; Tsesmelis, E.; Ulrichs, J.; Vacavant, L.; Valdata-Nappi, M.; Valuev, V.; Vannucci, F.; Varvell, K. E.; Veltri, M.; Vercesi, V.; Vidal-Sitjes, G.; Vieira, J.-M.; Vinogradova, T.; Weber, F. V.; Weisse, T.; Wilson, F. F.; Winton, L. J.; Yabsley, B. D.; Zaccone, H.; Zuber, K.; Zuccon, P.

    2001-05-01

    We report on a search for heavy neutrinos (?4) produced in the decay Ds-->??4 at the SPS proton target followed by the decay ?4-->??e+e- in the NOMAD detector. Both decays are expected to occur if ?4 is a component of ??. >From the analysis of the data collected during the 1996-1998 runs with 4.11019 protons on target, a single candidate event consistent with background expectations was found. This allows to derive an upper limit on the mixing strength between the heavy neutrino and the tau neutrino in the ?4 mass range from 10 to 190 MeV. Windows between the SN1987a and Big Bang Nucleosynthesis lower limits and our result are still open for future experimental searches. The results obtained are used to constrain an interpretation of the time anomaly observed in the KARMEN1 detector.

  17. Search for MSSM Higgs Bosons in Tau Final States with the D0 Detector

    SciTech Connect

    Yang, Wan-Ching; /Manchester U.

    2010-09-01

    The cross-section times branching ratio of the Higgs boson decaying to {tau}{sup +}{tau}{sup -} final state in the Standard Model (SM) is too small to play any role in the SM Higgs boson searches. This, however, is different in the Minimal Supersymmetric Standard Model (MSSM), which predicts two Higgs doublets leading to five Higgs bosons: a pair of charged Higgs boson (H{sup {+-}}); two neutral CP-even Higgs bosons (h,H) and a CP-odd Higgs boson (A). A search for the production of neutral Higgs bosons decaying into {tau}{sup +}{tau}{sup -} final states in p{bar p} collisions at a centre-of-mass energy of {radical}s = 1.96 TeV is presented in this thesis. One of the two {tau} leptons is required to decay into a muon while the other decays hadronically. The integrated luminosity is L = 1.0-5.36 fb{sup -1}, collected by the D0 experiment at the Fermilab Tevatron Collider from 2002 to 2009 in the Run II.

  18. Heterotypic seeding of Tau fibrillization by pre-aggregated Abeta provides potent seeds for prion-like seeding and propagation of Tau-pathology in vivo.

    PubMed

    Vasconcelos, Bruno; Stancu, Ilie-Cosmin; Buist, Arjan; Bird, Matthew; Wang, Peng; Vanoosthuyse, Alexandre; Van Kolen, Kristof; Verheyen, An; Kienlen-Campard, Pascal; Octave, Jean-Noël; Baatsen, Peter; Moechars, Diederik; Dewachter, Ilse

    2016-04-01

    Genetic, clinical, histopathological and biomarker data strongly support Beta-amyloid (Aβ) induced spreading of Tau-pathology beyond entorhinal cortex (EC), as a crucial process in conversion from preclinical cognitively normal to Alzheimer's Disease (AD), while the underlying mechanism remains unclear. In vivo preclinical models have reproducibly recapitulated Aβ-induced Tau-pathology. Tau pathology was thereby also induced by aggregated Aβ, in functionally connected brain areas, reminiscent of a prion-like seeding process. In this work we demonstrate, that pre-aggregated Aβ can directly induce Tau fibrillization by cross-seeding, in a cell-free assay, comparable to that demonstrated before for alpha-synuclein and Tau. We furthermore demonstrate, in a well-characterized cellular Tau-aggregation assay that Aβ-seeds cross-seeded Tau-pathology and strongly catalyzed pre-existing Tau-aggregation, reminiscent of the pathogenetic process in AD. Finally, we demonstrate that heterotypic seeded Tau by pre-aggregated Aβ provides efficient seeds for induction and propagation of Tau-pathology in vivo. Prion-like, heterotypic seeding of Tau fibrillization by Aβ, providing potent seeds for propagating Tau pathology in vivo, as demonstrated here, provides a compelling molecular mechanism for Aβ-induced propagation of Tau-pathology, beyond regions with pre-existing Tau-pathology (entorhinal cortex/locus coeruleus). Cross-seeding along functional connections could thereby resolve the initial spatial dissociation between amyloid- and Tau-pathology, and preferential propagation of Tau-pathology in regions with pre-existing 'silent' Tau-pathology, by conversion of a 'silent' Tau pathology to a 'spreading' Tau-pathology, observed in AD. PMID:26739002

  19. Exonic point mutations of human tau enhance its toxicity and cause characteristic changes in neuronal morphology, tau distribution and tau phosphorylation in the lamprey cellular model of tauopathy.

    PubMed

    Lee, Sangmook; Jung, Cheolwha; Lee, Gloria; Hall, Garth F

    2009-01-01

    Exonic mutations in the gene coding for human tau cause familial neurofibrillary degenerative diseases (tauopathies) which exhibit mutation-specific characteristics. It is thus unclear whether such mutations have similar effects on tau structure and function in vivo and if they act via similar cytopathological mechanisms in vulnerable neuron types. We have previously shown that overexpressing wild type human tau isoforms in identified giant neurons (ABCs) of the lamprey CNS results in characteristic, stereotyped cytopathological changes in these cells over several weeks. Here, we use this model to compare the cytopathological consequences of expressing wild type and exonic mutant tau isoforms (P301L, G272V, V337M, and R406W) at a high level of resolution. We show that each of the four exonic htau mutations tested accelerate degeneration in ABCs when compared to their WT parent isoforms, and that the patterns of human tau distribution, phosphorylation and cytopathology, while similar, vary characteristically from one another among both WT and mutant isoforms in a single identified neuron in situ. Our results therefore suggest that at least some of the differences between the effects of these mutations in humans are due to cell autonomous, mutation specific differences in the cytopathological mechanism of tau-induced neurodegeneration. PMID:19158426

  20. Intraneuronal tau aggregation precedes diffuse plaque deposition, but amyloid-β changes occur before increases of tau in cerebrospinal fluid.

    PubMed

    Braak, Heiko; Zetterberg, Henrik; Del Tredici, Kelly; Blennow, Kaj

    2013-11-01

    In comparison to the levels in age and gender-matched controls, reduced levels of pathological amyloid-β protein in cerebrospinal fluid routinely precede the onset of Alzheimer's disease-related symptoms by several years, whereas elevated soluble abnormal tau fractions (phosphorylated tau, total tau protein) in cerebrospinal fluid are detectable only with the onset and progression of clinical symptoms. This sequence of events in cerebrospinal fluid (amyloid-β changes detectable prior to abnormal tau changes) contrasts with that in which both proteins develop in the brain, where intraneuronal tau inclusions (pretangles, neurofibrillary tangles, neuropil threads) appear decades before the deposition of amyloid-β plaques (diffuse plaques, neuritic plaques). This viewpoint attempts to address questions arising in connection with this apparent sequential discrepancy-questions and issues for which there are currently no clear-cut answers. PMID:23756600

  1. Imbalance of Hsp70 family variants fosters tau accumulation

    PubMed Central

    Jinwal, Umesh K.; Akoury, Elias; Abisambra, Jose F.; O'Leary, John C.; Thompson, Andrea D.; Blair, Laura J.; Jin, Ying; Bacon, Justin; Nordhues, Bryce A.; Cockman, Matthew; Zhang, Juan; Li, Pengfei; Zhang, Bo; Borysov, Sergiy; Uversky, Vladimir N.; Biernat, Jacek; Mandelkow, Eckhard; Gestwicki, Jason E.; Zweckstetter, Markus; Dickey, Chad A.

    2013-01-01

    Dysfunctional tau accumulation is a major contributing factor in tauopathies, and the heat-shock protein 70 (Hsp70) seems to play an important role in this accumulation. Several reports suggest that Hsp70 proteins can cause tau degradation to be accelerated or slowed, but how these opposing activities are controlled is unclear. Here we demonstrate that highly homologous variants in the Hsp70 family can have opposing effects on tau clearance kinetics. When overexpressed in a tetracycline (Tet)-based protein chase model, constitutive heat shock cognate 70 (Hsc70) and inducible Hsp72 slowed or accelerated tau clearance, respectively. Tau synergized with Hsc70, but not Hsp72, to promote microtubule assembly at nearly twice the rate of either Hsp70 homologue in reconstituted, ATP-regenerating Xenopus extracts supplemented with rhodamine-labeled tubulin and human recombinant Hsp72 and Hsc70. Nuclear magnetic resonance spectroscopy with human recombinant protein revealed that Hsp72 had greater affinity for tau than Hsc70 (I/I0 ratio difference of 0.3), but Hsc70 was 30 times more abundant than Hsp72 in human and mouse brain tissue. This indicates that the predominant Hsp70 variant in the brain is Hsc70, suggesting that the brain environment primarily supports slower tau clearance. Despite its capacity to clear tau, Hsp72 was not induced in the Alzheimer's disease brain, suggesting a mechanism for age-associated onset of the disease. Through the use of chimeras that blended the domains of Hsp72 and Hsc70, we determined that the reason for these differences between Hsc70 and Hsp72 with regard to tau clearance kinetics lies within their C-terminal domains, which are essential for their interactions with substrates and cochaperones. Hsp72 but not Hsc70 in the presence of tau was able to recruit the cochaperone ubiquitin ligase CHIP, which is known to facilitate the ubiquitination of tau, describing a possible mechanism of how the C-termini of these homologous Hsp70 variants can differentially regulate tau triage. Thus, efforts to promote Hsp72 expression and inhibit Hsc70 could be therapeutically relevant for tauopathies.Jinwal, U. K., Akoury, E., Abisambra, J. F., O'Leary, J. C., III, Thompson, A. D., Blair, L. J., Jin, Y., Bacon, J., Nordhues, B. A., Cockman, M., Zhang, J., Li, P., Zhang, B., Borysov, S., Uversky, V. N., Biernat, J., Mandelkow, E., Gestwicki, J. E., Zweckstetter, M., Dickey, C. A. Imbalance of Hsp70 family variants fosters tau accumulation. PMID:23271055

  2. Histone deacetylase 6 inhibition improves memory and reduces total tau levels in a mouse model of tau deposition

    PubMed Central

    2014-01-01

    Introduction Tau pathology is associated with a number of age-related neurodegenerative disorders. Few treatments have been demonstrated to diminish the impact of tau pathology in mouse models and none are yet effective in humans. Histone deacetylase 6 (HDAC6) is an enzyme that removes acetyl groups from cytoplasmic proteins, rather than nuclear histones. Its substrates include tubulin, heat shock protein 90 and cortactin. Tubastatin A is a selective inhibitor of HDAC6. Modification of tau pathology by specific inhibition of HDAC6 presents a potential therapeutic approach in tauopathy. Methods We treated rTg4510 mouse models of tau deposition and non-transgenic mice with tubastatin (25mg/kg) or saline (0.9%) from 5 to 7months of age. Cognitive behavior analysis, histology and biochemical analysis were applied to access the effect of tubastatin on memory, tau pathology and neurodegeneration (hippocampal volume). Results We present data showing that tubastatin restored memory function in rTg4510 mice and reversed a hyperactivity phenotype. We further found that tubastatin reduced the levels of total tau, both histologically and by western analysis. Reduction in total tau levels was positively correlated with memory improvement in these mice. However, there was no impact on phosphorylated forms of tau, either by histology or western analysis, nor was there an impact on silver positive inclusions histologically. Conclusion Potential mechanisms by which HDAC6 inhibitors might benefit the rTg4510 mouse include stabilization of microtubules secondary to increased tubulin acetylation, increased degradation of tau secondary to increased acetylation of HSP90 or both. These data support the use of HDAC6 inhibitors as potential therapeutic agents against tau pathology. PMID:24576665

  3. Measurement of the inclusive branching fraction tau/sup -/. -->. nu/sub tau/. pi. /sup -/. pi. /sup 0/ + neutral meson(s)

    SciTech Connect

    Moses, W.W.

    1986-12-01

    This dissertation measures an inclusive branching fraction of (13.9 +- 2.0/sub -2.4//sup +2.1/)% for the decay tau/sup -/ ..-->.. nu/sub tau/..pi../sup -/..pi../sup 0/ + nh/sup 0/ where h/sup 0/ is a ..pi../sup 0/ or an eta and n greater than or equal to 1. The data sample, obtained with the TPC detector facility at PEP, corresponds to an integrated luminosity of 72 pb/sup -1/ at 29 GeV center of mass energy. The measured value for this branching fraction is somewhat greater than the theoretical prediction and, taking errors into account, resolves the present difference between the inclusive and the sum of the exclusive tau/sup -/ branching fractions into one charged prong. In addition, a lower limit of 8.3% (95% CL) is placed on the branching fraction B(tau/sup -/ ..-->.. nu/sub tau/..pi../sup -/..pi../sup 0/..pi../sup 0/).

  4. High statistics search for v{sub e}({bar v}{sub e}){r_arrow}v{sub {tau}}({bar v}{sub {tau}}) oscillations

    SciTech Connect

    Johnson, R.A.; Vakili, M.; Romosan, A.; Arroyo, C.G.; Bazarko, A.O.; Conrad, J.; Kim, J.H.; King, B.J.; Lefmann, W.C.; McNulty, C.; Mishra, S.R.; Quintas, P.Z.; Sciulli, F.J.; Seligman, W.G.; Shaevitz, M.H.; Spentzouris, P.; Stern, E.G.; Bernstein, R.H.; Lamm, M.J.; Marsh, W.; Yu, J.; Naples, D.; Bolton, T.; de Barbaro, L.; Schellman, H.; Drucker, R.B.; de Barbaro, P.; Bodek, A.; Budd, H.; Harris, D.A.; McFarland, K.S.; Sakumoto, W.K.; Yang, U.K.; Kinnel, T.; Smith, W.H.

    1999-02-01

    We present new limits on v{sub e}({bar v}{sub e}){r_arrow}v{sub {tau}}({bar v}{sub {tau}}) and v{sub e}({bar v}{sub e}){r_arrow}v{sub s} oscillations by searching for v{sub e} disappearance in the high-energy wideband CCFR neutrino beam. Sensitivity to v{sub {tau}} appearance comes from {tau} decay modes in which a large fraction of the energy deposited is electromagnetic. The beam is composed primarily of v{sub {mu}}({bar v}{sub {mu}}), but this analysis uses the 2.3{percent} v{sub e}({bar v}{sub e}) component of the beam. Electron neutrino energies range from 30 to 600 GeV and flight lengths vary from 0.9 to 1.4 km. This limit improves the sensitivity of existing limits for v{sub e}{r_arrow}v{sub {tau}} at high {Delta}m{sup 2} and obtains a lowest 90{percent} confidence upper limit in sin{sup 2}2{alpha} of 9.9{times}10{sup {minus}2} at {Delta}m{sup 2}{approximately}125 eV{sup 2}. {copyright} {ital 1998} {ital The American Physical Society}

  5. Regulatable transgenic mouse models of Alzheimer disease: onset, reversibility and spreading of Tau pathology.

    PubMed

    Hochgrfe, Katja; Sydow, Astrid; Mandelkow, Eva-Maria

    2013-09-01

    Accumulation of amyloidogenic proteins such as Tau is a hallmark of neurodegenerative diseases including Alzheimer disease and fronto-temporal dementias. To link Tau pathology to cognitive impairments and defects in synaptic plasticity, we created four inducible Tau transgenic mouse models with expression of pro- and anti-aggregant variants of either full-length human Tau (hTau40/?K280 and hTau40/?K280/PP) or the truncated Tau repeat domain (Tau(RD)/?K280 and Tau(RD)/?K280/PP). Here we review the histopathological features caused by pro-aggregant Tau, and correlate them with behavioral deficits and impairments in synaptic transmission. Both pro-aggregant Tau variants cause Alzheimer-like features, including synapse loss, mis-localization of Tau into the somatodendritic compartment, conformational changes and hyperphosphorylation. However, there is a clear difference in the extent of Tau aggregation and neurotoxicity. While pro-aggregant full-length hTau40/?K280 leads to a 'pre-tangle' pathology, the repeat domain Tau(RD)/?K280 causes massive formation of neurofibrillary tangles and neuronal loss in the hippocampus. However, both Tau variants cause co-aggregation of human and mouse Tau and similar functional impairments. Thus, earlier Tau pathological stages and not necessarily neurofibrillary tangles are critical for the development of cognitive malfunctions. Most importantly, memory and synapses recover after switching off expression of pro-aggregant Tau. The rescue of functional impairments correlates with the rescue of most Tau pathological changes and most strikingly the recovery of synapses. This implies that tauopathies as such are reversible, provided that amyloidogenic Tau is removed. Therefore, our Tau transgenic mice may serve as model systems for in vivo validation of therapeutic strategies and drug candidates with regard to cognition and synaptic function. PMID:23517246

  6. The DF Tau T Tauri Binary

    NASA Astrophysics Data System (ADS)

    Wright-Garba, Nuria Meilani Laure; Prato, Lisa A.; Allen, Thomas; Biddle, Lauren; Avilez, Ian; Schaefer, Gail

    2016-01-01

    Most stars form in multiple systems. Despite this, there are observed differences in properties of stars formed within close proximity of each other. This makes obtaining images and spectra of resolved components in systems for individual analysis desirable. DF Tau is a young, low-mass, visual binary in the Taurus star-forming region with a semi-major axis of ~13 AU. With Adaptive Optics, we are able to acquire high-resolution spectroscopic and imaging data of the primary and secondary stars. We find the primary and secondary differ in a number of characteristics, including vsini and disk presence. This is in spite of the stars having identical spectral types. We are in the process of mapping the ~44-year orbit, and here we present our latest imaging and spectroscopic data.

  7. On planet formation in HL Tau

    NASA Astrophysics Data System (ADS)

    Dipierro, Giovanni; Price, Daniel; Laibe, Guillaume; Hirsh, Kieran; Cerioli, Alice; Lodato, Giuseppe

    2015-10-01

    We explain the axisymmetric gaps seen in recent long-baseline observations of the HL Tau protoplanetary disc with the Atacama Large Millimetre/Submillimetre Array (ALMA) as being due to the different response of gas and dust to embedded planets in protoplanetary discs. We perform global, three-dimensional dusty smoothed particle hydrodynamics calculations of multiple planets embedded in dust/gas discs which successfully reproduce most of the structures seen in the ALMA image. We find a best match to the observations using three embedded planets with masses of 0.2, 0.27 and 0.55 MJ in the three main gaps observed by ALMA, though there remain uncertainties in the exact planet masses from the disc model.

  8. Probing lepton nonuniversality in tau neutrino scattering

    NASA Astrophysics Data System (ADS)

    Liu, Hongkai; Rashed, Ahmed; Datta, Alakabha

    2015-10-01

    Recently hints of lepton flavor nonuniversality emerged in the BABAR and LHCb experiments. In this paper we propose tests of lepton universality in ?? scattering. To parametrize the new physics we adopt an effective Lagrangian approach and consider the neutrino deep inelastic scattering processes ??+N ?? +X and ??+N ?? +X where we assume the largest new physics effects are in the ? sector. We also consider an explicit leptoquark model in our calculations. In order to make comparison with the standard model and also in order to cancel out the uncertainties of the parton distribution functions, we consider the ratio of total and differential cross sections of tau-neutrino to muon-neutrino scattering. We find new physics effects that can possibly be observed at the proposed Search for Hidden Particles (SHiP) experiment at CERN.

  9. WFPC-2 Observations of the Circumstellar Nebulosity of T Tau and HL Tau

    NASA Astrophysics Data System (ADS)

    Stapelfeldt, Karl R.; Burrows, C. J.; Krist, J.; Trauger, J.; Ballester, G.; Casertano, S.; Clarke, J.; Crisp, D.; Gallagher, J.; Griffiths, R.; Hester, J.; Hoessel, J.; Holtzman, J.; Mould, J.; Scowen, P.; Westphal, J.; Watson, A.

    1994-05-01

    T Tauri lies on an arc of reflection nebulosity which extends approximately 3('') N and 2('') SW from the star. This nebula has a characteristic width of 0.5('') , is concave open toward the nearby Burnham's Nebula, and is closely aligned with the optical polarization vector of the system. The morphology T Tau's edge-brightened cometary nebula is similar to models of scattered light from a flared, optically thick disk observed from 45 degrees above the equator plane. No optical counterpart to the infrared companion is seen to a limiting magnitude of V= 23. WFPC2 images of HL Tauri show that this object is entirely reflection nebulosity at optical wavelengths. No stellar source is visible to a limiting magnitude of V= 26, a result which dictates a significant upward revision of the luminosity and mass estimates for HL Tau. The V-I color of the nebula is dominated by foreground extinction, with only small internal color changes. The bright core of the nebula has an east-west elongation of 1('') and has an unusual morphology. We will discuss the implications of these results for i). HL Tau's stellar type and ii). models for the distribution of the circumstellar matter.

  10. Tau leaping of stiff stochastic chemical systems via local central limit approximation

    SciTech Connect

    Yang, Yushu; Rathinam, Muruhan

    2013-06-01

    Stiffness manifests in stochastic dynamic systems in a more complex manner than in deterministic systems; it is not only important for a time-stepping method to remain stable but it is also important for the method to capture the asymptotic variances accurately. In the context of stochastic chemical systems, time stepping methods are known as tau leaping. Well known existing tau leaping methods have shortcomings in this regard. The implicit tau method is far more stable than the trapezoidal tau method but underestimates the asymptotic variance. On the other hand, the trapezoidal tau method which estimates the asymptotic variance exactly for linear systems suffers from the fact that the transients of the method do not decay fast enough in the context of very stiff systems. We propose a tau leaping method that possesses the same stability properties as the implicit method while it also captures the asymptotic variance with reasonable accuracy at least for the test system S{sub 1}?S{sub 2}. The proposed method uses a central limit approximation (CLA) locally over the tau leaping interval and is referred to as the LCLA-?. The CLA predicts the mean and covariance as solutions of certain differential equations (ODEs) and for efficiency we solve these using a single time step of a suitable low order method. We perform a mean/covariance stability analysis of various possible low order schemes to determine the best scheme. Numerical experiments presented show that LCLA-? performs favorably for stiff systems and that the LCLA-? is also able to capture bimodal distributions unlike the CLA itself. The proposed LCLA-? method uses a split implicit step to compute the mean update. We also prove that any tau leaping method employing a split implicit step converges in the fluid limit to the implicit Euler method as applied to the fluid limit differential equation.

  11. TOC1: Characterization of a Selective Oligomeric Tau Antibody

    PubMed Central

    Ward, Sarah M.; Himmelstein, Diana S.; Lancia, Jody K.; Fu, Yifan; Patterson, Kristina R.; Binder, Lester I.

    2016-01-01

    The work presented herein addresses a specific portion of the tau pathology, pre-fibrillar oligomers, now thought to be important pathological components in Alzheimer’s disease and other neurodegenerative tauopathies. In previous work, we generated an antibody against purified recombinant cross-linked tau dimers, called Tau Oligomeric Complex 1 (TOC1). TOC1 recognizes tau oligomers and its immunoreactivity is elevated in Alzheimer’s disease brains. In this report, we expand upon the previous study to show that TOC1 selectively labels tau oligomers over monomers or polymers, and that TOC1 is also reactive in other neurodegenerative tauopathies. Using a series of deletion mutants spanning the tau molecule, we further demonstrate that TOC1 has one continuous epitope located within amino acids 209–224, in the so-called proline rich region. Together with the previous study, our data indicates that TOC1 is a conformation-dependent antibody whose epitope is revealed upon dimerization and oligomerization, but concealed again as polymers form. This characterization of the TOC1 antibody further supports its potential as a powerful biochemical tool that can be used to better investigate the involvement of tau in neurodegenerative diseases. PMID:23979027

  12. Structure and Pathology of Tau Protein in Alzheimer Disease

    PubMed Central

    Kolarova, Michala; García-Sierra, Francisco; Bartos, Ales; Ricny, Jan; Ripova, Daniela

    2012-01-01

    Alzheimer's disease (AD) is the most common type of dementia. In connection with the global trend of prolonging human life and the increasing number of elderly in the population, the AD becomes one of the most serious health and socioeconomic problems of the present. Tau protein promotes assembly and stabilizes microtubules, which contributes to the proper function of neuron. Alterations in the amount or the structure of tau protein can affect its role as a stabilizer of microtubules as well as some of the processes in which it is implicated. The molecular mechanisms governing tau aggregation are mainly represented by several posttranslational modifications that alter its structure and conformational state. Hence, abnormal phosphorylation and truncation of tau protein have gained attention as key mechanisms that become tau protein in a pathological entity. Evidences about the clinicopathological significance of phosphorylated and truncated tau have been documented during the progression of AD as well as their capacity to exert cytotoxicity when expressed in cell and animal models. This paper describes the normal structure and function of tau protein and its major alterations during its pathological aggregation in AD. PMID:22690349

  13. Dysregulation of Tau Phosphorylation in Mouse Brain during Excitotoxic Damage

    PubMed Central

    Liang, Zhihou; Liu, Fei; Iqbal, Khalid; Grundke-Iqbal, Inge; Gong, Cheng-Xin

    2010-01-01

    Glutamate receptor-mediated excitotoxicity is thought to contribute to the development of Alzheimer’s disease (AD), but the underlying mechanism is unknown. In this study, we investigated the dynamic changes of tau phosphorylation and tau-related protein kinases and protein phosphatase 2A (PP2A) in the mouse brain during excitotoxicity induced by intraperitoneal injection of 20 mg/kg kainic acid (KA). We found that KA-induced excitotoxicity led to transient dephosphorylation of tau (within 6 hr post-injection), followed by sustained hyperphosphorylation of tau at multiple sites that are hyperphosphorylated in AD brain. The initial dephosphorylation of tau may result from activation of PP2A, and the sustained hyperphosphorylation may be due mainly to activation of cdk5 and down-regulation of PP2A during the later phase. Because abnormal hyperphosphorylation of tau plays a crucial role in neurodegeneration and in the formation of neurofibrillary tangles, our results suggest that glutamate receptor–mediated excitotoxicity might contribute to AD partially via promoting abnormal hyperphosphorylation of tau in AD brain. PMID:19363259

  14. Dysregulation of tau phosphorylation in mouse brain during excitotoxic damage.

    PubMed

    Liang, Zhihou; Liu, Fei; Iqbal, Khalid; Grundke-Iqbal, Inge; Gong, Cheng-Xin

    2009-01-01

    Glutamate receptor-mediated excitotoxicity is thought to contribute to the development of Alzheimer's disease (AD), but the underlying mechanism is unknown. In this study, we investigated the dynamic changes of tau phosphorylation and tau-related protein kinases and protein phosphatase 2A (PP2A) in the mouse brain during excitotoxicity induced by intraperitoneal injection of 20 mg/kg kainic acid (KA). We found that KA-induced excitotoxicity led to transient dephosphorylation of tau (within 6 hr post-injection), followed by sustained hyperphosphorylation of tau at multiple sites that are hyperphosphorylated in AD brain. The initial dephosphorylation of tau may result from activation of PP2A, and the sustained hyperphosphorylation may be due mainly to activation of cdk5 and down-regulation of PP2A during the later phase. Because abnormal hyperphosphorylation of tau plays a crucial role in neurodegeneration and in the formation of neurofibrillary tangles, our results suggest that glutamate receptor-mediated excitotoxicity might contribute to AD partially via promoting abnormal hyperphosphorylation of tau in AD brain. PMID:19363259

  15. Elimination of spurious eigenvalues in the Chebyshev tau spectral method

    NASA Technical Reports Server (NTRS)

    Mcfadden, G. B.; Murray, B. T.; Boisvert, R. F.

    1989-01-01

    Spectral methods have been used to great advantage in hydrodynamic stability calculations; the concepts are described in Orszag's seminal application of the Chebyshev tau method to the Orr-Sommerfeld equation for plane Poiseuille flow in 1971. Orszag discusses both the Chebyshev Galerkin and the Chebyshev tau methods, but presents results for the tau method, which is easier to implement than the Galerkin method. The tau method has the disadvantage that two unstable eigenvalues are produced that are artifacts of the discretization. An extremely simple modification to the Chebyshev tau method is presented which eliminates the spurious eigenvalues. First a simplified model of the Orr-Sommerfeld equation discussed by Gottlieb and Orszag was studied. Then the Chebyshev tau method is considered, which has two spurious eigenvalues, and then a modification which eliminates them is described. Finally, results for the Orr-Sommerfeld equation are considered where the modified tau method also eliminates the spurious eigenvalues. The simplicity of the modification makes it a convenient alternative to other approaches to the problem.

  16. Tau neutrino astronomy in GeV energies

    NASA Astrophysics Data System (ADS)

    Athar, H.; Lee, Fei-Fan; Lin, Guey-Lin