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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. Decays of the heavy lepton, tau (1785)

    SciTech Connect

    Blocker, C.A.

    1980-04-01

    The structure of the weak hadronic current coupled to the tau is investigated via some of the hadronic decays of the tau. The vector current coupling is determined by measuring the tau ..-->.. rho ..nu../sub tau/ branching ratio. The axial-vector coupling is determined by measuring the tau ..-->.. ..pi.. ..nu../sub tau/ branching ratio. The Cabibbo structure of the hadronic current is established by observing the decay tau ..-->.. K*(890)..nu../sub tau/ and measuring its branching ratio. The branching ratios for the decays tau ..-->.. e anti ..nu../sub e/..nu../sub tau/ and tau ..-->.. ..mu.. anti ..nu../sub ..mu../..nu../sub tau/ are measured as a normalization for the hadronic decays and as a check on the validity of the measurements. The leptonic branching ratios agree well with previous experiments. From a kinematic fit to the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, an upper limit (95% confidence level) of 245 MeV is placed on the tau neutrino mass. From a simultaneous fit of the center of mass energy dependence of the tau production cross section and the pion energy spectrum in the decay tau ..-->.. ..pi.. ..nu../sub tau/, the tau mass is determined to be 1.787 +- .010 GeV/c. All properties of the tau measured here are consistent with it being a sequential lepton coupled to the ordinary weak hadronic current.

  5. Tau decays into K* mesons

    NASA Astrophysics Data System (ADS)

    Albrecht, H.; Hamacher, T.; Hofmann, R. P.; Kirchhoff, T.; Mankel, R.; Nau, A.; Nowak, S.; Schröder, H.; Schulz, H. D.; Walter, M.; Wurth, R.; Hast, C.; Kapitza, H.; Kolanoski, H.; Kosche, A.; Lange, A.; Lindner, A.; Schieber, M.; Siegmund, T.; Spaan, B.; Thurn, H.; Töpfer, D.; Wegener, D.; Eckstein, P.; Schubert, K. R.; Schwierz, R.; Waldi, R.; Reim, K.; Wegener, H.; Eckmann, R.; Kuipers, H.; Mai, O.; Mundt, R.; Oest, T.; Reiner, R.; Schmidt-Parzefall, W.; Stiewe, J.; Werner, S.; Ehret, K.; Hofmann, W.; Hüpper, A.; Knöpfle, K. T.; Spengler, J.; Krieger, P.; Macfarlane, D. B.; Saull, P. R. B.; Tzamariudaki, K.; van de Water, R. G.; Yoon, T.-S.; Frankl, C.; Reßing, D.; Schmidtler, M.; Schneider, M.; Weseler, S.; Kernel, G.; Križan, P.; Križnič, E.; Podobnik, T.; Živko, T.; Balagura, V.; Belyaev, I.; Schechelnitsky, S.; Danilov, M.; Doutskoy, A.; Gershtein, Yu.; Golutvin, A.; Korolko, I.; Kostina, G.; Litvintsev, D.; Lubimov, V.; Pakhlov, P.; Semenov, S.; Snizhko, A.; Tichomirov, I.; Zaitsev, Yu.

    1995-06-01

    Using the ARGUS detector at the storage ring DORIS II we have measured τ decays into three charged mesons containing K * mesons. Exploiting the good particle identification capabilities of the detector we have determined the following branching ratios:Brleft( {tau ^ - to overline {K^{*0} } π ^ - v_tau } right) = left( {0.25 ± 0.10 ± 0.05} right)% , B r (τ-→ K *0 K - v τ)= (0.20±0.05±0.04)%, and B r (τ-→ K *- X 0 v τ) =(1.15±0.15-0.18 +0.13)%.

  6. Tau Decays at BaBar

    SciTech Connect

    Hast, Carsten; /SLAC

    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. Measurements of the decays tau/sup -/. -->. rho/sup -/. nu. /sub tau/, tau/sup -/. -->. pi. /sup -/. nu. /sub tau/ and tau/sup -/. -->. K*-(892). nu. /sub tau/ using the MARK II detector at SPEAR

    SciTech Connect

    Dorfan, J.

    1981-04-01

    Measurements of the branching fractions for the Cabibbo favored decays tau/sup -/ ..-->.. rho/sup -/ ..-->.. ..pi../sup -/..nu../sub tau/ and the Cabibbo suppressed decay mode tau/sup -/ ..-->.. K*/sup -/ (892)..nu../sub tau/ are presented. The energy dependence of the tau/sup +/tau/sup -/ production cross section is obtained for the decays tau/sup -/ ..-->.. rho/sup -/..nu../sub tau/ and these spectra agree well with the classification of the tau/sup -/ as a spin-1/2 point particle. Fits to the production cross section yield a measurement of M/sub tau/ = (1787 +- 10) MeV/c/sup 2/ for the tau mass. Ninety-five percent confidence upper limits for the forbidden decay tau/sup -/ ..-->.. K*/sup -/(1430)..nu../sub tau/ and the tau neutrino mass are presented.

  8. 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.

  9. 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}.

  10. 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.

  11. Precision measurements of tau lepton decays

    NASA Astrophysics Data System (ADS)

    Nugent, Ian M.

    Using data collected with the BABAR detector at the SLAC PEP-II electron-positron storage ring operating at a centre-of-mass energy near 10.58 GeV, the branching fractions B (tau-- → pi--pi --pi+nutau) = (8.83 +/- 0.01 +/- 0.13)%, B (tau-- → K--pi --pi+nutau) = (0.273 +/- 0.002 +/- 0.009)%, B (tau-- → K--pi --K+nutau) = (0.1346 +/- 0.0010 +/- 0.0036)%, and B (tau-- → K-- K--K +nutau) = (1.58 +/- 0.13 +/- 0.12) x 10--5 are measured where the uncertainties are statistical and systematic, respectively. The invariant mass distribution for the tau -- → pi--pi--pi +nutau, tau-- → K--pi--pi+nu tau, tau-- → K --pi--K+nu tau and tau-- → K --K--K +nutau decays are unfolded to correct for detector effects. A measurement of B (tau-- → φpi--nu tau) = (3.42 +/- 0.55 +/- 0.25) x 10--5 , a measurement of B (tau-- → φK --nutau) = (3.39 +/- 0.20 +/- 0.28) x 10--5 and an upper limit on B (tau-- → K-- K--K +nutau [ex.φ]) ≤ 2.5 x 10--6 90%CL are determined from a binned maximum likelihood fit of the tau-- → K-- pi--K+nu tau and tau-- → K --K--K +nutau K+K -- invariant mass distributions. The branching ratio Bt-→K -nt Bt-→p -nt is measured to be (6.531 +/- 0.056 +/- 0.093) x 10 --2 from which |Vus| is determined to be 0.2255 +/- 0.0023. The branching ratio Bt-→m -ntn¯ mB t-→e-nt n¯e = (9.796 +/- 0.016 +/- 0.035) x 10--1 is measured enabling a precision test of the Standard Model assumption of charged current lepton universality, gmge = 1.0036 +/- 0.0020. The branching ratios Bt-→K -nt Bt-→e- ntn¯ e = (3.882 +/- 0.032 +/- 0.056) x 10--2 , and Bt-→p -nt Bt-→e- ntn¯ e = (5.945 +/- 0.014 +/- 0.061) x 10--1 are measured which provide additional tests of charged current lepton universality, gtgm p = 0.9856 +/- 0.0057 and gtgm K = 0.9827 +/- 0.0086 which can be combined to give gtgm p/K = 0.9850 +/- 0.0054. Any deviation of these measurements from the expected Standard Model values would be an indication of new physics.

  12. Tau neutrino component to tritium beta decay

    SciTech Connect

    Snyderman, N.J.

    1995-06-01

    A framework is given for explaining anomalous results of neutrino mass experiments that measure the high energy electron spectrum of tritium {beta} decay. The experimental results have been fit to a negative neutrino mass square. We show that there is a consistent phenomenological interpretation due to a positive mass tau neutrino component of the {beta} decay spectrum, with strong near threshold final state interactions with the He nucleus. If this enhancement is due to new interactions between low energy tau neutrinos and nuclei, then the tritium 0 decay experiments could be used as detectors for cosmic background tau neutrinos. The model predicts a distinctive spectrum shape that is consistent with a recent high statistics LLNL experiment. A fit to the experiment gives a tau neutrino mass of 23 eV. Tau neutrinos of this mass would dominate the mass of the universe. Requirements for a theoretical model are given, as well as models that realize different aspects of these requirements. While qualitatively successful, the theoretical models have such severe quantitative difficulties that the accuracy of the molecular physics of the T-{sup 3}He ion, assumed in the analysis of the experimental data, is called into question.

  13. Hadronic Tau Decays at BaBar

    SciTech Connect

    Nugent, I.M.; /Victoria U.

    2007-10-25

    Precision measurements of the exclusive branching fraction {tau}{sup -} {yields} K{sup -}{pi}{sup 0}{nu}{sub {tau}} and {tau}{sup -} {yields} h{sup -}h{sup -}h{sup +}{nu}{sub {tau}}, where the h represent either a pion or a kaon, from the BABAR Experiment are presented. The branching fraction for {tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu}{sub {tau}} is the first resonant plus non-resonant measurement of this mode and the branching fraction {tau}{sup -} {yields} {phi}{pi}{sup -}{nu}{sub {tau}} is also a first measurement. In addition we present the new measurement of the branching fraction of {tau}{sup -} {yields} {phi}K{sup -}{nu}{sub {tau}}.

  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. 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

  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. 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.; /more authors..

    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.

  19. 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.

  20. 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.

  1. Enhanced tau neutrino appearance through invisible decay

    NASA Astrophysics Data System (ADS)

    Pagliaroli, Giulia; Di Marco, Natalia; Mannarelli, Massimo

    2016-06-01

    The decay of neutrino mass eigenstates leads to a change of the conversion and survival probability of neutrino flavor eigenstates. Exploiting the recent results released by the long-baseline OPERA experiment we perform the statistical investigation of the neutrino invisible decay hypothesis in the νμ→ντ appearance channel. We find that the neutrino decay provides an enhancement of the expected tau appearance signal with respect to the standard oscillation scenario for the long-baseline OPERA experiment. The increase of the νμ→ντ conversion probability by the decay of one of the mass eigenstates is due to a reduction of the "destructive interference" among the different massive neutrino components. Despite data showing a very mild preference for invisible decays with respect to the oscillations only hypothesis, we provide an upper limit for the neutrino decay lifetime in this channel of τ3/m3≳1.3 ×10-13 s /eV at the 90% confidence level.

  2. 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; Béquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, 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; Côté, 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 Vaissière, Ch; Hamon, O; Leruste, Ph; Malclès, 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; Haire, M; Biesiada, J; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Ricciardi, S; Roethel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Hast, C; Hryn'ova, T; Innes, W R; Kaminski, J; Kelsey, M H; Kim, H; Kim, P; Kocian, M L; Leith, D W G S; Li, S; Luitz, S; Luth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; 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; Wagner, A P; 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; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    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

  3. 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.

  4. 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.

  5. 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.

  6. Wess-Zumino current and the structure of the decay tau- -->K- pi- K+ nu tau.

    PubMed

    Coan, T E; Gao, Y S; Liu, F; Stroynowski, R; Artuso, M; Boulahouache, C; Blusk, S; Butt, J; Dambasuren, E; Dorjkhaidav, O; Haynes, J; Menaa, N; Mountain, R; Muramatsu, H; Nandakumar, R; Redjimi, R; Sia, R; Skwarnicki, T; Stone, S; Wang, J C; Zhang, Kevin; Mahmood, A H; Csorna, S E; Bonvicini, G; Cinabro, D; Dubrovin, M; Bornheim, A; Lipeles, E; Pappas, S P; Shapiro, A; Weinstein, A J; Briere, R A; Chen, G P; Ferguson, T; Tatishvili, G; Vogel, H; Watkins, M E; Adam, N E; Alexander, J P; Berkelman, K; Boisvert, V; Cassel, D G; Duboscq, J E; Ecklund, K M; Ehrlich, R; Galik, R S; Gibbons, L; Gittelman, B; Gray, S W; Hartill, D L; Heltsley, B K; Hsu, L; Jones, C D; Kandaswamy, J; Kreinick, D L; Kuznetsov, V E; Magerkurth, A; Mahlke-Krüger, H; Meyer, T O; Patterson, J R; Pedlar, T K; Peterson, D; Pivarski, J; Riley, D; Sadoff, A J; Schwarthoff, H; Shepherd, M R; Sun, W M; Thayer, J G; Urner, D; Wilksen, T; Weinberger, M; Athar, S B; Avery, P; Breva-Newell, L; Potlia, V; Stoeck, H; Yelton, J; Eisenstein, B I; Gollin, G D; Karliner, I; Lowrey, N; Naik, P; Sedlack, C; Selen, M; Thaler, J J; Williams, J; Edwards, K W; Besson, D; Gao, K Y; Gong, D T; Kubota, Y; Li, S Z; Poling, R; Scott, A W; Smith, A; Stepaniak, C J; Urheim, J; Metreveli, Z; Seth, K K; Tomaradze, A; Zweber, P; Arms, K; Eckhart, E; Gan, K K; Gwon, C; Severini, H; Skubic, P; Asner, D M; Dytman, S A; Mehrabyan, S; Mueller, J A; Nam, S; Savinov, V; Huang, G S; Miller, D H; Pavlunin, V; Sanghi, B; Shibata, E I; Shipsey, I P J; Adams, G S; Chasse, M; Cummings, J P; Danko, I; Napolitano, J; Cronin-Hennessy, D; Park, C S; Park, W; Thayer, J B; Thorndike, E H

    2004-06-11

    We present the first study of the vector (Wess-Zumino) current in tau(-)-->K-pi-K+nu(tau) decay using data collected with the CLEO III detector at the Cornell Electron Storage Ring. We determine the quantitative contributions to the decay width from the vector and axial vector currents. Within the framework of a model by Kühn and Mirkes, we identify the quantitative contributions to the total decay rate from the intermediate states omegapi, rho(')pi, and K*K. PMID:15245150

  7. 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.

  8. Lepton flavor violating {tau} and B decays and heavy neutrinos

    SciTech Connect

    He Xiaogang

    2004-12-01

    We study lepton flavor violating (LFV) {tau} and B decays in models with heavy neutrinos to constrain the mixing matrix parameters U{sub {tau}}{sub N}. We find that the best current constraints when the heavy neutrinos are purely left handed come from LFV radiative {tau} decay modes. To obtain competitive constraints in LFV B decay, it is necessary to probe b{yields}X{sub s}{tau}{sup {+-}}e{sup {+-}} at the 10{sup -7} level. When the heavy neutrinos have both left- and right-handed couplings, the mixing parameters can be constrained by studying LFV B decay modes and LFV {tau} decay into three charged leptons. We find that the branching ratios B({tau}{sup {+-}}{yields}l{sub 1}{sup {+-}}l{sub 2}{sup {+-}}l{sub 3}{sup {+-}}), B(B{sub s}{yields}{tau}{sup {+-}}e{sup {+-}}) and B(b{yields}X{sub s}l{sub 1}{sup {+-}}l{sub 2}{sup {+-}}) need to be probed at the 10{sup -8} level in order to constrain the mixing parameters beyond what is known from unitarity.

  9. Disentangling perturbative and power corrections in precision tau decay analysis

    SciTech Connect

    Gorbunov, D.S.; Pivovarov, A.A.

    2005-01-01

    Hadronic tau decay precision data are analyzed with account of both perturbative and power corrections of high orders within QCD. It is found that contributions of high order power corrections are essential for extracting a numerical value for the strange quark mass from the data on Cabibbo suppressed tau decays. We show that with inclusion of new five-loop perturbative corrections in the analysis the convergence of perturbation theory remains acceptable only for few low order moments. We obtain m{sub s}(M{sub {tau}})=130{+-}27 MeV in agreement with previous estimates.

  10. 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).

  11. 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; Béquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, 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; Côté, 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 Vaissière, Ch; Hamon, O; Leruste, Ph; Malclès, 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; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Roethel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; 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; Luitz, S; Luth, V; Lynch, H L; Macfarlane, D B; Marsiske, H; Messner, R; Muller, D R; Nelson, S; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Yi, K; Young, C C; Ziegler, V; Burchat, P R; Edwards, A J; Majewski, S A; Miyashita, T S; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    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

  12. 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.

  13. 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.

  14. 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.

  15. 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.

  16. Measurement of the Semileptonic B-bar->D{sup (*)}{tau}{nu}-bar{sub {tau}} Decays at BABAR

    SciTech Connect

    Lopes Pegna, David

    2010-02-10

    Semileptonic B meson decays into final states containing the tau lepton are of interesting as they provide information on the Standard Model as well as a window on new physics effects. We present results on B-bar->D{sup (*)}taunu-bar{sub tau} decays where the second B in the event is fully reconstructed.

  17. 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; Schröder, 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; Yèche, 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; Marsiske, H; Messner, R; Muller, D R; Neal, H; Nelson, S; O'Grady, C P; Ofte, I; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; West, C A; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Young, C C; Ziegler, V; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Bellis, M; Burchat, P R; Edwards, A J; Miyashita, T S; Ahmed, S; Alam, M S; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Soffer, A; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Wray, B C; Drummond, B W; Izen, J M; Lou, X C; Bianchi, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Choi, H H F; Hamano, K; King, G J; Kowalewski, R; Lewczuk, M J; Lindsay, C D; Locke, C B; Nugent, I M; Roney, J M; Sobie, R J; Gershon, T J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Puccio, E M T; Band, H R; Chen, X; Dasu, S; Flood, K T; Pan, Y; Prepost, R; Vuosalo, C O; Wu, S L

    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

  18. Evidence for the decay tau/sup -/. -->. pi. /sup -/eta nu/sub tau/

    SciTech Connect

    Repond, J.

    1987-01-01

    The inclusive production of eta mesons in tau lepton decay has been studied using the High Resolution Spectrometer at the PEP e/sup +/e/sup -/ facility. The data sample corresponds to an integrated luminosity of 300 pb/sup -1/ and the storage ring was operated at ..sqrt..s = 29 GeV. The eta production appears to be only compatible with the decay tau/sup -/ ..-->.. ..pi../sup -/eta nu, which violates isospin and G-parity conservation. The branching ratio of 5.1 +- 1.5% explains much of the current discrepancy between the one-prong topological branching ratio and the sum of the individual one-prong modes. Various checks to test the validity of the signal are described.

  19. 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.

  20. 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.

  1. 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.

  2. 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)%.

  3. Studies of tau- to h- h- h+ nu and tau- to K- pi0 nu Decays at BaBar

    SciTech Connect

    Nugent, I.M.; /Victoria U.

    2007-10-24

    We present preliminary inclusive branching fraction measurements of {tau}{sup -} {yields} h{sup -}h{sup -}h{sup +}{nu} (h = {pi} or K) and {tau}{sup -} K{sup -}{pi}{sup 0}{nu} decay modes using a sample of {tau}-pair events collected by the BABAR detector at the SLAC PEP-II asymmetric e{sup +}e{sup -} storage ring. The branching fractions of {tau}{sup -} {yields} {pi}{sup -}{pi}{sup -}{pi}{sup +}, {tau}{sup -} {yields} K{sup -}{pi}{sup -}{pi}{sup +}{nu}, and {tau}{sup -} {yields} K{sup -}{pi}{sup -}K{sup +}{nu} are measured with higher precision than previously published results and the inclusive branching fraction {tau}{sup -} {yields} K{sup -}K{sup -}K{sup +}{nu} is measured for the first time. In addition, the first measurement of the branching fraction {tau}{sup -} {yields} {pi}{sup -}{phi}{nu} and the measurement of the branching fraction {tau}{sup -} {yields} K{sup -}{phi}{nu} are determined by means of a binned maximum likelihood fit to the K{sup +}K{sup -} invariant mass distribution. These branching fractions are extracted by means of a migration matrix that accounts for the cross contamination between the {tau}{sup -} {yields} h{sup -}h{sup -}h{sup +}{nu} modes. The preliminary {tau}{sup -} {yields} K{sup -}{pi}{sup 0}{nu} branching fraction and invariant mass distributions are also presented in this paper.

  4. Search for Tau-Lepton Decays to Seven Or More Pions With BaBar

    SciTech Connect

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

    2007-11-02

    We report the results of searches for several decay modes of the {tau}-lepton with {ge} 7 pions in the final state using 207 x 10{sup 6} {tau}-pairs collected with the BaBar detector. For the decays with 7 charged pions in the final state we find the following 90% CL upper limits: B({tau}{sup -} {yields} 4{pi}{sup -}3{pi}{sup +}({pi}{sup 0}){nu}{sub {tau}}) < 3.0 x 10{sup -7}, B({tau}{sup -} {yields} 4{pi}{sup -}3{pi}{sup +}{nu}{sub {tau}}) < 4.3 x 10{sup -7} and B({tau}{sup -} {yields}) B({tau}{sup -} {yields} 4{pi}{sup -}3{pi}{sup +}{pi}{sup 0}{nu}{sub {tau}}) < 2.5 x 10{sup -7}. We also search for the decay {tau}{sup -} {yields} 3{pi}{sup -}2{pi}{sup +}2{pi}{sup 0}{nu}{sub {tau}} and report a 90% CL upper limit of < 3.4 x 10{sup -6} for its branching fraction. Finally, we search for the exclusive final state {tau}{sup -} {yields} 2{sigma}{pi}{sup -}{nu}{sub {tau}} and find a 90% CL upper limit for its branching fraction of < 5.4 x 10{sup -7}.

  5. A Search for Neutrinoless Tau Decays to Three Leptons

    SciTech Connect

    Kolb, Jeffrey A.

    2008-06-01

    Using approximately 350 million τ+τ- 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 β}(τ → ℓℓℓ) in the range (4-8) x 10-8.

  6. The one charged particle decay modes of the tau

    SciTech Connect

    Perl, M.L.

    1987-11-01

    Tables of measurements of the total branching fraction of tau lepton decays to modes with one charged particle are given along with the major individual branching fractions. The reason a combination of measurements and calculations is needed to display the discrepancy is described briefly. It is argued that uncertainties in measurements of the branching fractions for multiple photon decay modes prevent complete reliance on experiment. The multiple photon modes are discussed in more detail. Present research on experimental technique problems relative to the apparent discrepancy is summarized. (LEW)

  7. 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.

  8. 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; Höcker, 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; Côté, 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; Chauveau, J; David, P; Del Buono, L; de la Vaissière, Ch; Hamon, O; Hartfiel, B L; Leruste, Ph; Malclès, J; Ocariz, J; Roos, L; Therin, G; Gladney, L; Biasini, M; Covarelli, R; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J 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; del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Tehrani, F Safai; Voena, C; Ebert, M; Schröder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Ricciardi, S; Wilson, F F; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; de Monchenault, G Hamel; Kozanecki, W; Legendre, M; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dujmic, D; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Leith, D W G S; Li, S; Luitz, S; Luth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Pulliam, T; 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; Wagner, A P; Weaver, M; Weinstein, A J R; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Pappagallo, M; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Flood, K T; Hollar, J J; Kutter, P E; Mellado, B; Mihalyi, A; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Yu, Z; Neal, 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

  9. Precision Measurements of Tau Lepton Decays

    SciTech Connect

    Nugent, Ian M.

    2008-01-01

    Using data collected with the BABAR detector at the SLAC PEP-II electron-positron storage ring operating at a centre-of-mass energy near 10.58 GeV, the branching fractions B(τ- → π-π-π+ντ) =(8.83±0.01±0.13)%, B(τ- → K-π-π+ντ) =(0.273± 0.002 ± 0.009)%, B(τ- → K-π-K+ντ) =(0.1346 ± 0.0010 ± 0.0036)%, and B(τ- → K-K-K+ντ) =(1.58 ± 0.13 ± 0.12) × 10-5 are measured where the uncertainties are statistical and systematic, respectively. The invariant mass distribution for the τ- → π-π-π+ντ , τ- → K-π-π+ντ , τ- → K-π-K+ντ and τ- → K-K-K+ντ decays are unfolded to correct for detector effects. A measurement of B(τ- → φπ-ντ ) =(3.42±0.55±0.25)×10-5, a measurement of B(τ- → φK-ντ) =(3.39±0.20±0.28)× 10-5 and an upper limit on B(τ- → K-K-K+ντ [ex.φ]) ≤ 2.5 × 10-6@90%CL are determined from a binned maximum likelihood fit of the τ- → K-π-K+ντ and τ- → K-K-K+ντ K+K- invariant mass distributions. The branching ratio B(τ-→K-ντ )/ B(τ-→π-ντ ) is measured to be (6.531±0.056±0.093)×10-2 from which |Vus| is determined to be 0.2255 ± 0.0023. The branching ratio B(τ-→μ-ντ $\\bar{v}$μ)/ B(τ-→e-ντ $\\bar{v}$e) =(9.796 ± 0.016 ± 0.035) × 10-1 is measured enabling a precision test of the Standard Model assumption of

  10. 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.

  11. Tau polarisation at LEP

    NASA Astrophysics Data System (ADS)

    Alemany, Ricard

    1999-04-01

    The measurements of the tau polarisation at LEP I are reviewed. Special emphasis is given to the new preliminary results presented at this conference. The ALEPH collaboration has studied the polarisation as a function of the polar angle using a new method based on the tau direction reconstruction and fully exploiting the angular correlations. A second traditional approach, based on the single tau decays has been also developed. The DELPHI collaboration has also studied the full data sample using an individual tau decay method and an inclusive hadronic selection. The results from the four experiments are presented with discussion of the compatibility among the methods and experiments.

  12. 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.

  13. Determination of the CP properties of the Higgs boson from data on tau-lepton-decay products in the process e{sup +}e{sup -} {sup {yields}} {tau}{sup +}{tau}{sup -}{nu}{nu}-bar

    SciTech Connect

    Likhoded, A. A.

    2008-03-15

    The process e{sup +}e{sup -} {sup {yields}} {tau}{sup +}{tau}{sup -}v{nu}-bar, which is highly sensitive to anomalous H{tau}{tau} interaction, is investigated within a model involving a new pseudoscalar Higgs boson. It is shown that the problem of separating the contributions of the scalar and pseudoscalar states of the Higgs boson can be solved via taking into account the polarizations of final-state particles. The inclusion of cascade tau-lepton decays makes it possible to determine reliably the CP state of the Higgs boson and to pinpoint the magnitude and sign of respective coupling constants.

  14. 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.).

  15. Searches for Lepton Flavor Violation in the Decays tau{sup +}-->e{sup +}-{gamma} and {tau}{sup +}-->{mu}{sup +}-{gamma}

    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.; Hooberman, B.; Kerth, L. T.; Kolomensky, Yu. G.

    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{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 we set upper limits on the branching fractions of B(tau{sup +}-->e{sup +}-{gamma})<3.3x10{sup -8} and B({tau}{sup +}-->{mu}{sup +}-{gamma})<4.4x10{sup -8} at 90% confidence level.

  16. LFV in semileptonic {tau} decays and {mu}-e conversion in nuclei in SUSY-seesaw

    SciTech Connect

    Arganda, E.; Herrero, M.; Rodriguez-Sanchez, A.; Teixeira, A. M.

    2008-11-23

    Here we review the main results of LFV in the semileptonic tau decays {tau}{yields}{mu}PP(PP = {pi}{sup +}{pi}{sup -}, {pi}{sup 0}{pi}{sup 0}, K{sup +}K{sup -}, K{sup 0}K-bar{sup 0}), {tau}{yields}{mu}P(P = {pi},{eta},{eta}'), and {tau}{yields}{mu}V(V = {rho},{phi}) as well as in {mu}-e conversion in nuclei within SUSY-seesaw scenarios, and compare our predictions with the present experimental bounds.

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

    PubMed

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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

  18. 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.

  19. The investigation of CP violation through the decay of polarized tau leptons

    SciTech Connect

    Tsai, Y.S.

    1996-03-01

    Under the assumption that CP violation is caused by exchange of a new boson, the author proposes to measure the magnitudes and CP-violating phases of the coupling constants of this boson to five different vertices in tau decay. This can be accomplished by studying the decays of polarized tau leptons produced at an e{sup +} e{sup {minus}} collider whose beams are polarized. He points out that CP violation in the tau decay tests most directly the assumption in the standard theory that the imaginary numbers in the mass matrix is the sole cause of CP violation.

  20. 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.

  1. 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.

  2. Search for lepton flavor violating decays tau to l \\omega (l = e, mu)

    SciTech Connect

    Collaboration, The BABAR; Aubert, B.

    2007-11-12

    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{sup -1} of e{sup +}e{sup -} 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 {beta}({tau}{sup {+-}} {yields} e{sup {+-}}{omega}) < 1.1 x 10{sup -7} and {beta}({tau}{sup {+-}} {yields} {mu}{sup {+-}}{omega}) < 1.0 x 10{sup -7} at 90% confidence level.

  3. 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.

  4. 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}.

  5. 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.

  6. 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

  7. 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.

  8. 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.

  9. Study of Exclusive Semileptonic B Meson Decays toTau Leptons

    SciTech Connect

    Mazur, Michael A.; /SLAC /UC, Santa Barbara

    2007-10-15

    We present the results of a search for four exclusive semileptonic decays B {yields} D{sup (*)}{tau}{sup -}{bar {nu}}{sub {tau}} in 209 fb{sup -1} of data collected with the BABAR detector, corresponding to 232 million e+e- {yields} {Upsilon}(4S) {yields} B{bar B} events. We select events with a D{sup (*)} meson and a light lepton (e or {mu}) recoiling against a fully-reconstructed B meson. We perform a fit to the lepton spectrum and missing mass squared to discriminate signal events from backgrounds, predominantly B {yields} D{sup (*)}{tau}{sup -}{bar {nu}}{sub {tau}}. A control sample of identified D**{ell}{sup -}{bar {nu}}{sub {ell}} events is included in the fit to estimate the background contribution from these decays. We measure {beta}(B {yields} D{sub {tau}{nu}}) = (0.86{+-}0.24{+-}0.11{+-}0.06)% and {beta}(B {yields} D*{sub {tau}{nu}}) = (1.62{+-}0.31{+-}0.10{+-}0.05)%, where the errors are statistical, systematic, and normalization-mode related, respectively, and where the results are expressed for the {bar B}{sup 0} lifetime.

  10. 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.

  11. The investigation of CP violation through the decay of polarized tau leptons II

    SciTech Connect

    Tsai, Y.S.

    1996-05-01

    Under the assumption that CP violation is caused by exchange of anew boson, the authors propose to measure the magnitudes and CP-violating phases of the coupling constants of this boson to five different vertices in tau decay. This can be accomplished by studying the decay of polarized tau leptons produced at an e{sup +}e{sup {minus}} collider whose beams are polarized. These five coupling constants could be used to construct a future theory of CP violation. If CP is violated in any channel of tau decay, it will imply that there exists a new charged boson other than the W boson responsible for CP violation. It will also imply that CP violation is much more prevalent than the standard theory predicts and this may enable one to understand the preponderance of matter over antimatter in the present universe.

  12. 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.

  13. Search for doubly charged Higgs bosons with lepton-flavor-violating decays involving tau leptons.

    PubMed

    Aaltonen, T; Adelman, J; Akimoto, T; Albrow, M G; Alvarez González, B; Amerio, S; Amidei, D; Anastassov, A; Annovi, A; Antos, J; Aoki, M; Apollinari, G; Apresyan, A; Arisawa, T; Artikov, A; Ashmanskas, W; Attal, A; Aurisano, A; Azfar, F; Azzi-Bacchetta, P; Azzurri, P; Bacchetta, N; Badgett, W; Barbaro-Galtieri, A; Barnes, V E; Barnett, B A; Baroiant, S; Bartsch, V; Bauer, G; Beauchemin, P-H; Bedeschi, F; Bednar, P; Behari, S; Bellettini, G; Bellinger, J; Belloni, A; Benjamin, D; Beretvas, A; Beringer, J; Berry, T; Bhatti, A; Binkley, M; Bisello, D; Bizjak, I; Blair, R E; Blocker, C; Blumenfeld, B; Bocci, A; Bodek, A; Boisvert, V; Bolla, G; Bolshov, A; Bortoletto, D; Boudreau, J; Boveia, A; Brau, B; Bridgeman, A; Brigliadori, L; Bromberg, C; Brubaker, E; Budagov, J; Budd, H S; Budd, S; Burkett, K; Busetto, G; Bussey, P; Buzatu, A; Byrum, K L; Cabrera, S; Campanelli, M; Campbell, M; Canelli, F; Canepa, A; Carlsmith, D; Carosi, R; Carrillo, S; Carron, S; Casal, B; Casarsa, M; Castro, A; Catastini, P; Cauz, D; 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; Ciobanu, C I; Ciocci, M A; Clark, A; Clark, D; Compostella, G; Convery, M E; Conway, J; Cooper, B; Copic, K; Cordelli, M; Cortiana, G; 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 Lentdecker, G; De Lorenzo, G; Dell'Orso, M; Demortier, L; Deng, J; Deninno, M; De Pedis, D; Derwent, P F; 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; 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; Forrester, S; Franklin, M; Freeman, J C; Furic, I; Gallinaro, M; Galyardt, J; Garberson, F; Garcia, J E; Garfinkel, A F; Genser, K; Gerberich, H; Gerdes, D; Giagu, S; Giakoumopolou, V; Giannetti, P; Gibson, K; Gimmell, J L; Ginsburg, C M; Giokaris, N; Giordani, M; Giromini, P; Giunta, M; Glagolev, V; Glenzinski, D; Gold, M; Goldschmidt, N; Golossanov, A; Gomez, G; Gomez-Ceballos, G; Goncharov, M; González, O; Gorelov, I; Goshaw, A T; Goulianos, K; Gresele, A; Grinstein, S; Grosso-Pilcher, C; Grundler, U; Guimaraes da Costa, J; Gunay-Unalan, Z; Haber, C; Hahn, K; Hahn, S R; Halkiadakis, E; Hamilton, A; Han, B-Y; Han, J Y; Handler, R; Happacher, F; Hara, K; Hare, D; Hare, M; Harper, S; Harr, R F; Harris, R M; Hartz, M; Hatakeyama, K; Hauser, J; Hays, C; Heck, M; Heijboer, A; Heinemann, B; 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; Huston, J; Incandela, J; Introzzi, G; Iori, M; Ivanov, A; Iyutin, B; James, E; Jayatilaka, B; Jeans, D; Jeon, E J; 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; Kerzel, U; Khotilovich, V; Kilminster, B; Kim, D H; Kim, H S; Kim, J E; Kim, M J; Kim, S B; Kim, S H; Kim, Y K; Kimura, N; Kirsch, L; Klimenko, S; Klute, M; Knuteson, B; Ko, B R; Koay, S A; Kondo, K; Kong, D J; Konigsberg, J; Korytov, A; Kotwal, A V; Kraus, J; Kreps, M; Kroll, J; Krumnack, N; Kruse, M; Krutelyov, V; Kubo, T; Kuhlmann, S E; Kuhr, T; Kulkarni, N P; 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; LeCompte, T; Lee, J; Lee, J; Lee, Y J; Lee, S W; Lefèvre, R; Leonardo, N; Leone, S; Levy, S; Lewis, J D; Lin, C; Lin, C S; Linacre, J; Lindgren, M; Lipeles, E; Lister, A; Litvintsev, D O; Liu, T; Lockyer, N S; Loginov, A; Loreti, M; Lovas, L; Lu, R-S; Lucchesi, D; Lueck, J; Luci, C; Lujan, P; Lukens, P; Lungu, G; Lyons, L; Lys, J; Lysak, R; Lytken, E; Mack, P; MacQueen, D; Madrak, R; Maeshima, K; Makhoul, K; Maki, T; Maksimovic, P; Malde, S; Malik, S; Manca, G; Manousakis, A; Margaroli, F; Marino, C; Marino, C P; Martin, A; Martin, M; Martin, V; Martínez, M; Martínez-Ballarín, R; Maruyama, T; Mastrandrea, P; Masubuchi, T; Mattson, M E; Mazzanti, P; McFarland, K S; McIntyre, P; McNulty, R; Mehta, A; Mehtala, P; Menzemer, S; Menzione, A; Merkel, P; Mesropian, C; Messina, A; Miao, T; Miladinovic, N; Miles, J; Miller, R; Mills, C; Milnik, M; Mitra, A; Mitselmakher, G; Miyake, H; Moed, S; Moggi, N; Moon, C S; Moore, R; Morello, M; Movilla Fernandez, P; Mülmenstädt, 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; Neu, C; Neubauer, M S; Nielsen, J; Nodulman, L; Norman, M; Norniella, O; Nurse, E; Oh, S H; Oh, Y D; Oksuzian, I; Okusawa, T; Oldeman, R; Orava, R; Osterberg, K; Pagan Griso, S; Pagliarone, C; Palencia, E; Papadimitriou, V; Papaikonomou, A; Paramonov, A A; Parks, B; Pashapour, S; Patrick, J; Pauletta, G; Paulini, M; Paus, C; Pellett, D E; Penzo, A; Phillips, T J; Piacentino, G; Piedra, J; Pinera, L; Pitts, K; Plager, C; Pondrom, L; Portell, X; Poukhov, O; Pounder, N; Prakoshyn, F; Pronko, A; Proudfoot, J; Ptohos, F; Punzi, G; Pursley, J; Rademacker, J; Rahaman, A; Ramakrishnan, V; Ranjan, N; Redondo, I; Reisert, B; Rekovic, V; Renton, P; Rescigno, M; Richter, S; Rimondi, F; Ristori, L; Robson, A; Rodrigo, T; Rogers, E; Rolli, S; Roser, R; Rossi, M; Rossin, R; Roy, P; Ruiz, A; Russ, J; Rusu, V; Saarikko, H; Safonov, A; Sakumoto, W K; Salamanna, G; Saltó, O; Santi, L; Sarkar, S; Sartori, L; Sato, K; Savoy-Navarro, A; Scheidle, T; Schlabach, P; Schmidt, E E; Schmidt, M A; Schmidt, M P; Schmitt, M; Schwarz, T; Scodellaro, L; Scott, A L; Scribano, A; Scuri, F; Sedov, A; Seidel, S; Seiya, Y; Semenov, A; Sexton-Kennedy, L; Sfyrla, A; Shalhout, S Z; Shapiro, M D; Shears, T; Shepard, P F; Sherman, D; Shimojima, M; Shochet, M; Shon, Y; Shreyber, I; Sidoti, A; Sinervo, P; Sisakyan, A; Slaughter, A J; Slaunwhite, J; Sliwa, K; Smith, J R; Snider, F D; Snihur, R; Soderberg, M; Soha, A; Somalwar, S; Sorin, V; Spalding, J; Spinella, F; Spreitzer, T; Squillacioti, P; Stanitzki, M; St Denis, R; Stelzer, B; Stelzer-Chilton, O; Stentz, D; Strologas, J; Stuart, D; Suh, J S; Sukhanov, A; Sun, H; Suslov, I; Suzuki, T; Taffard, A; Takashima, R; Takeuchi, Y; Tanaka, R; Tecchio, M; Teng, P K; Terashi, K; Thom, J; Thompson, A S; Thompson, G A; Thomson, E; Tipton, P; Tiwari, V; Tkaczyk, S; Toback, D; Tokar, S; Tollefson, K; Tomura, T; Tonelli, D; Torre, S; Torretta, D; Tourneur, S; Trischuk, W; Tu, Y; Turini, N; Ukegawa, F; Uozumi, S; Vallecorsa, S; van Remortel, N; Varganov, A; Vataga, E; Vázquez, F; Velev, G; Vellidis, C; Veszpremi, V; Vidal, M; Vidal, R; Vila, I; Vilar, R; Vine, T; Vogel, M; Volobouev, I; Volpi, G; Würthwein, F; Wagner, P; Wagner, R G; Wagner, R L; Wagner-Kuhr, J; Wagner, W; Wakisaka, T; Wallny, R; Wang, S M; Warburton, A; Waters, D; Weinberger, M; Wester, W C; Whitehouse, B; Whiteson, D; Wicklund, A B; Wicklund, E; Williams, G; Williams, H H; Wilson, P; Winer, B L; Wittich, P; Wolbers, S; Wolfe, C; Wright, T; Wu, X; Wynne, S M; Yagil, A; Yamamoto, K; Yamaoka, J; Yamashita, T; Yang, C; Yang, U K; Yang, Y C; Yao, W M; Yeh, G P; Yoh, J; Yorita, K; Yoshida, T; Yu, G B; Yu, I; Yu, S S; Yun, J C; Zanello, L; Zanetti, A; Zaw, I; Zhang, X; Zheng, Y; Zucchelli, S

    2008-09-19

    We search for pair production of doubly charged Higgs particles (H+/- +/-) followed by decays into electron-tau (etau) and muon-tau (mutau) pairs using data (350 pb(-1) collected from [over]pp collisions at sqrt[s]=1.96 TeV by the CDF II experiment. We search separately for cases where three or four final-state leptons are detected, and combine results for exclusive decays to left-handed etau (mutau) pairs. We set an H+/- +/- lower mass limit of 114(112) GeV/c(2) at the 95% confidence level. PMID:18851361

  14. 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.; Åkesson, 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.; Åsman, 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 Guimarães 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. 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    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.

  15. Reconstruction of hadronic decay products of tau leptons with the ATLAS experiment

    NASA Astrophysics Data System (ADS)

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C.; Zeng, Q.; Zengel, K.; Zenin, O.; Ženiš, T.; Zerwas, D.; Zhang, D.; Zhang, F.; Zhang, G.; Zhang, H.; Zhang, J.; Zhang, L.; Zhang, R.; Zhang, X.; Zhang, Z.; Zhao, X.; Zhao, Y.; Zhao, Z.; Zhemchugov, A.; Zhong, J.; Zhou, B.; Zhou, C.; Zhou, L.; Zhou, L.; Zhou, M.; Zhou, N.; Zhu, C. G.; Zhu, H.; Zhu, J.; Zhu, Y.; Zhuang, X.; Zhukov, K.; Zibell, A.; Zieminska, D.; Zimine, N. I.; Zimmermann, C.; Zimmermann, S.; Zinonos, Z.; Zinser, M.; Ziolkowski, M.; Živković, L.; Zobernig, G.; Zoccoli, A.; zur Nedden, M.; Zurzolo, G.; Zwalinski, L.

    2016-05-01

    This paper presents a new method of reconstructing the individual charged and neutral hadrons in tau decays with the ATLAS detector. The reconstructed hadrons are used to classify the decay mode and to calculate the visible four-momentum of reconstructed tau candidates, significantly improving the resolution with respect to the calibration in the existing tau reconstruction. The performance of the reconstruction algorithm is optimised and evaluated using simulation and validated using samples of Z→ τ τ and Z(→ μ μ )+jets events selected from proton-proton collisions at a centre-of-mass energy √{s}=8 {TeV}, corresponding to an integrated luminosity of 5 fb^{-1}.

  16. Reconstruction of hadronic decay products of tau leptons with the ATLAS experiment

    DOE PAGESBeta

    Aad, G.; Abbott, B.; Abdallah, J.; Abdinov, O.; Aben, R.; Abolins, M.; AbouZeid, O. S.; Abramowicz, H.; Abreu, H.; Abreu, R.; et al

    2016-05-25

    This document presents a new method of reconstructing the individual charged and neutral hadrons in tau decays with the ATLAS detector. The reconstructed hadrons are used to classify the decay mode and to calculate the visible four-momentum of reconstructed tau candidates, significantly improving the resolution with respect to the calibration in the existing tau reconstruction. The performance of the reconstruction algorithm is optimised and evaluated using simulation and validated using samples of Z → ττ and Z(→ μμ)+jets events selected from proton–proton collisions at a centre-of-mass energy √s = 8 TeV, corresponding to an integrated luminosity of 5 fb-1.

  17. 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.

  18. TAU2012 Summary

    NASA Astrophysics Data System (ADS)

    Pich, Antonio

    2014-08-01

    The main highlights discussed at TAU2012 are briefly summarized. Besides the standard topics on lepton physics covered also at previous conferences (universality, QCD tests, Vus determination from τ decay, g - 2, ν oscillations, lepton-flavour violation), the τ lepton is playing now a very important role in searches for new physics phenomena.

  19. Measurement of the branching fractions and the invariant mass distributions for {tau}{sup -{yields}}h{sup -}h{sup +}h{sup -{nu}}{sub {tau}}decays

    SciTech Connect

    Lee, M. J.; Kim, S. K.; Ryu, S.; Aihara, H.; Iwasaki, M.; Arinstein, K.; Aulchenko, V.; Bondar, A.; Eidelman, S.; Epifanov, D.; Gabyshev, N.; Garmash, A.; Kuzmin, A.; Poluektov, A.; Shebalin, V.; Shwartz, B.; Usov, Y.; Vinokurova, A.; Zhilich, V.; Zhulanov, V.

    2010-06-01

    We present a study of {tau}{sup -{yields}{pi}-{pi}+{pi}-{nu}}{sub {tau}}, {tau}{sup -{yields}}K{sup -{pi}+{pi}-{nu}}{sub {tau}}, {tau}{sup -{yields}}K{sup -}K{sup +{pi}-{nu}}{sub {tau}}, and {tau}{sup -{yields}}K{sup -}K{sup +}K{sup -{nu}}{sub {tau}} decays using a 666 fb{sup -1} data sample collected with the Belle detector at the KEKB asymmetric-energy e{sup +}e{sup -} collider at and near a center-of-mass energy of 10.58 GeV. The branching fractions are measured to be B({tau}{sup -{yields}{pi}-{pi}+{pi}-{nu}}{sub {tau}})=(8.42{+-}0.00{sub -0.25}{sup +0.26})x10{sup -2}, B({tau}{sup -{yields}}K{sup -{pi}+{pi}-{nu}}{sub {tau}})=(3.30{+-}0.01{sub -0.17}{sup +0.16})x10{sup -3}, B({tau}{sup -{yields}}K{sup -}K{sup +{pi}-{nu}}{sub {tau}})=(1.55{+-}0.01{sub -0.05}{sup +0.06})x10{sup -3}, and B({tau}{sup -{yields}}K{sup -}K{sup +}K{sup -{nu}}{sub {tau}})=(3.29{+-}0.17{sub -0.20}{sup +0.19})x10{sup -5}, where the first uncertainty is statistical and the second is systematic. These branching fractions do not include contributions from modes in which a {pi}{sup +{pi}-} pair originates from a K{sub S}{sup 0} decay. We also present the unfolded invariant mass distributions for these decays.

  20. What Renders TAU Toxic

    PubMed Central

    Götz, Jürgen; 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 Alzheimer’s disease (AD) forms insoluble, filamentous aggregates. When 20 years after TAU’s 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 TAU’s 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

  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.; /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. /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. /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

    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. Tau leptons and the decay H → τ τ at CMS

    NASA Astrophysics Data System (ADS)

    Nehrkorn, Alexander

    2016-12-01

    The tau lepton and its reconstruction at CMS are briefly described. This is followed by a summary of the searches for a standard model Higgs boson and neutral Higgs bosons from the minimal supersymmetric extension of the standard model decaying into pairs of tau leptons performed by the CMS Collaboration. The data samples used in these searches were collected during the first running period of the LHC and contain 4.9 fb-1 at √ {s}=7 {TeV} and 19.7 fb-1 at √ {s}=8 {TeV}.

  3. 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.

  4. 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.

  5. 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}.

  6. Pathways of tau fibrillization.

    PubMed

    Kuret, Jeff; Chirita, Carmen N; Congdon, Erin E; Kannanayakal, Theresa; Li, Guibin; Necula, Mihaela; Yin, Haishan; Zhong, Qi

    2005-01-01

    New methods for analyzing tau fibrillization have yielded insights into the biochemical transitions involved in the process. Here we review the parallels between the sequential progression of tau fibrillization observed macroscopically in Alzheimer's disease (AD) lesions and the pathway of tau aggregation observed in vitro with purified tau preparations. In addition, pharmacological agents for further dissection of fibrillization mechanism and lesion formation are discussed. PMID:15615636

  7. 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.

  8. 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; Béquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, 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; Côté, 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 Vaissière, Ch; Hamon, O; Leruste, Ph; Malclès, 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; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Roethel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; 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; Luitz, S; Luth, V; Lynch, H L; Macfarlane, D B; Marsiske, H; Messner, R; Muller, D R; Nelson, S; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Ziegler, V; Burchat, P R; Edwards, A J; Majewski, S A; Miyashita, T S; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    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

  9. Tau longitudinal polarization in B{yields}D{tau}{nu} and its role in the search for the charged Higgs boson

    SciTech Connect

    Tanaka, Minoru; Watanabe, Ryoutaro

    2010-08-01

    We study the longitudinal polarization of the tau lepton in B{yields}D{tau}{nu} decay. After discussing possible sensitivities of {tau} decay modes to the {tau} polarization, we examine the effect of charged Higgs boson on the {tau} polarization in B{yields}D{tau}{nu}. We find a relation between the decay rate and the {tau} polarization, and clarify the role of the {tau} polarization measurement in the search for the charged Higgs boson.

  10. 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}.

  11. 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.

  12. 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.

  13. 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.

  14. 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).

  15. 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.

  16. Untangling tau imaging.

    PubMed

    Villemagne, Victor L; Okamura, Nobuyuki; Rowe, Christopher C

    2016-01-01

    In vivo imaging of tau deposits is providing a better understanding of the temporal and spatial tau deposition in the brain, allowing a more comprehensive insight into the causes, diagnoses, and potentially treatment of tauopathies such as Alzheimer's disease, progressive supranuclear palsy, corticobasal syndrome, chronic traumatic encephalopathy, and some variants of frontotemporal lobar degeneration. The assessment of tau deposition in the brain over time will allow a deeper understanding of the relationship between tau and other variables such as cognition, genotype, and neurodegeneration, as well as assessing the role tau plays in ageing. Preliminary human studies suggest that tau imaging could also be used as a diagnostic, prognostic, and theranostic biomarker, as well as a surrogate marker for target engagement, patient recruitment, and efficacy monitoring for disease-specific therapeutic trials. PMID:27489878

  17. 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.

  18. 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.

  19. Five-body leptonic decays of muon and tau leptons

    NASA Astrophysics Data System (ADS)

    Flores-Tlalpa, A.; Castro, G. López; Roig, P.

    2016-04-01

    We study the five-body decays {μ}-to {e}-{e}+{e}-{ν}_{μ }{overline{ν}}_e and {τ}-to {ℓ}-{ℓ}^' +}{ℓ}^' -}{ν}_{τ }{overline{ν}}_{ℓ } for ℓ, ℓ ' = e, μ within the Standard Model (SM) and in a general effective field theory description of the weak interactions at low energies. We compute the branching ratios and compare our results with two previous — mutually discrepan — SM calculations. By assuming a general structure for the weak currents we derive the expressions for the energy and angular distributions of the three charged leptons when the decaying lepton is polarized, which will be useful in precise tests of the weak charged current at Belle II. In these decays, leptonic T-odd correlations in triple products of spin and momenta — which may signal time reversal violation in the leptonic sector — are suppressed by the tiny neutrino masses. Therefore, a measurement of such T-violating observables would be associated to neutrinoless lepton flavor violating (LFV) decays, where this effect is not extremely suppressed. We also study the backgrounds that the SM five-lepton lepton decays constitute to searches of LFV L - → ℓ - ℓ '+ ℓ '- decays. Searches at high values of the invariant mass of the ℓ '+ ℓ '- pair look the most convenient way to overcome the background.

  20. 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.

  1. 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; Béquilleux, J; D'Orazio, A; Davier, M; Grosdidier, G; Höcker, 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; Côté, 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 Vaissière, Ch; Hamon, O; Leruste, Ph; Malclès, 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; Elmer, P; Lau, Y P; Lu, C; Olsen, J; Smith, A J S; Telnov, A V; Baracchini, E; Bellini, F; Cavoto, G; Del Re, D; Di Marco, E; Faccini, R; Ferrarotto, F; Ferroni, F; Gaspero, M; Jackson, P D; Li Gioi, L; Mazzoni, M A; Morganti, S; Piredda, G; Polci, F; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Castelli, G; Franek, B; Olaiya, E O; Roethel, W; Wilson, F F; Emery, S; Escalier, M; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; 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; Luitz, S; Luth, V; Lynch, H L; Macfarlane, D B; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ofte, I; Perazzo, A; Perl, M; Pulliam, T; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; Wisniewski, W J; Wittgen, M; Wright, D H; Yarritu, A K; Yi, K; Young, C C; Ziegler, V; Burchat, P R; Edwards, A J; Majewski, S A; Miyashita, T S; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Band, H R; Chen, X; Dasu, S; Flood, K T; Hollar, J J; Kutter, P E; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Neal, H

    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

  2. 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

  3. 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.

  4. a Measurement of Tau Polarization

    NASA Astrophysics Data System (ADS)

    Walsh, Arthur Michael

    At ALEPH, polarized tau pairs are produced in e^+e^- annihilations at the Z peak. The polarization depends on the tau production angle and is measured by spin analyzing tau decays in the modes tauto{rm e}nu |nu, tautomunu |nu, tautopinu, tautorhonu and tauto{rm a}_1nu . This leads to a measurement of the Z couplings to taus and electrons, {cal A} _tau and {cal A }_{rm e}, where {cal A}_{l} = 2g_sp {V}{l}g_sp{A}{l }/(g_sp{V}{l}^2 + g_sp{A}{l}^2). The values obtained using the 1992 data are { cal A}_tau = 0.129 +/- 0.016 +/- 0.010 and {cal A} _{rm e} = 0.136 +/- 0.022 +/- 0.007, where the first error is statistical and the second is systematic. Assuming electron-tau universality leads to {cal A}_{ rm e-tau} = 0.131 +/- 0.013 +/- 0.006. This result has been combined with the published ALEPH result for the 1990 and 1991 data for a measurement of the effective weak mixing angle sin ^2 theta_sp{W}{ rm eff} = 0.2334 +/- 0.0014.

  5. 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.

  6. 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.

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

    DOE PAGESBeta

    Khachatryan, Vardan

    2016-01-29

    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.

  8. 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.

  9. 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.

  10. Search for a Standard Model Higgs boson in the $\\tau\\tau$ decay channel produced in $p\\bar{p}$ collisions at $\\sqrt{s}$ = 1.96 TeV at Tevatron

    SciTech Connect

    Totaro, Pierluigi

    2011-01-01

    This thesis describes the search for the Standard Model Higgs boson decaying to tau lepton pairs, in the Tevatron proton-antiproton collisions at a center of mass energy $\\sqrt{s}$ = 1.96 TeV. The search is based on approximately 2.3 fb$^{-1}$ of CDF Run II data and is performed by considering the following signal processes: WH($\\rightarrow\\tau\\tau$), ZH($\\rightarrow\\tau\\tau$), qHq'$\\rightarrow$q$\\tau\\tau$q' and gg$\\rightarrow$H$\\rightarrow\\tau\\tau$. Events are selected by requiring an hadronic tau and one isolated electron or muon, coming from the leptonic decay of one of the two taus. In addition, at least one calorimeter jet must be present in the final state. We expect 921.8$\\pm$48.9 background events in the 1 jet channel and 159.4$\\pm$11.6 in the $\\ge$ 2 jets channel, while in data we observe 965 and 166 events, respectively. In order to improve the search sensitivity we employ a multivariate technique, based on a set of Boosted Decision Trees trained to get the best sep aration between signal and the dominant sources of background. We observe no evidence for a Higgs boson signal and therefore we set a 95\\% confidence level (C.L.) upper limit on the cross section relative to the SM predictions ($\\sigma/\\sigma_{\\mathrm{SM}}$). Results are presented for the Higgs boson mass varying from M$_\\mathrm{H}$ = 100 GeV/$c^2$ to M$_\\mathrm{H}$ = 150 GeV/$c^2$. For the mass hypothesis of 120 GeV/c$^2$ the observed limit is 27.2, while the corresponding expected value is 23.4$^{+9.8}_{-6.4}$.

  11. 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

  12. Tau Flavour Violation at the LHC

    SciTech Connect

    Carquin, E.

    2009-04-17

    We study the relevance of neutrino oscillation data for sparticle decays that violate the {tau} lepton number at the LHC, in the context of the Constrained Minimal Supersymmetric Extension of the Standard Model (CMSSM) and in SU(5) extensions of the theory. We study the conditions required for {chi}{sub 2}{yields}{chi}+{tau}{sup {+-}}{mu}{sup {+-}} decays to yield observable tau flavour violation, for cosmologically interesting values of the neutralino relic density. We present detailed studies of the relevant supersymmetric parameter space and pay particular emphasis to signals from tau hadronisation, that are analysed using PYTHIA event simulation.

  13. 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.

  14. 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

  15. 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.

  16. 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 -}}.

  17. Tau physics 1994: A theoretical perspective

    SciTech Connect

    Marciano, W.J.

    1994-11-01

    In this paper I describe some recent advances in tau physics and discuss their implications from a theoretical perspective. The examples I have chosen include e-{mu}-{tau} universality, QCD studies, anomalous electroweak dipole moments, and forbidden decays. That list is by no means exhaustive. It should, however, demonstrate the breath of tau physics, describe some interesting new results, and point out the potential for future advances.

  18. Neuropathology of Frontotemporal Lobar Degeneration–Tau (FTLD-Tau)

    PubMed Central

    Dickson, Dennis W.; Kouri, Naomi; Murray, Melissa E.; Josephs, Keith A.

    2011-01-01

    A clinically and pathologically heterogeneous type of frontotemporal lobar degeneration has abnormal tau pathology in neurons and glia (FTLD-tau). Familial FTLD-tau is usually due to mutations in the tau gene (MAPT). Even FTLD-tau determined by MAPT mutations ha s clinical and pathologic heterogeneity. Tauopathies are subclassified according to the predominant species of tau that accumulates, with respect to alternative splicing of MAPT, with tau proteins containing 3 (3R) or 4 repeats (4R) of ~ 32 amino acids in the microtubule binding domain. In Pick's disease (PiD), 3R tau predominates, whereas 4R tau is characteristic of corticobasal degeneration (CBD) and progressive supranuclear palsy (PSP). Depending upon the specific mutation in MAPT, familial FTLD-tau can have 3R, 4R or a combination of 3R and 4R tau. PiD is the least common FTLD-tau characterized by neuronal Pick bodies in a stereotypic neuroanatomical distribution. PSP and CBD are more common than PiD and have extensive clinical and pathologic overlap, with no distinctive clinical syndrome or biomarker that permits their differentiation. Diagnosis rests upon postmortem examination of the brain and demonstration of globose tangles, oligodendroglial coiled bodies and tufted astrocytes in PSP or threads, pretangles and astrocytic plaques in CBD. The anatomical distribution of tau pathology determines the clinical presentation of PSP and CBD, as well as PiD. The basis for this selective cortical vulnerability in FTLD-tau is unknown. PMID:21720721

  19. 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

  20. 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.

  1. 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.

  2. Confronting QCD with the experimental hadronic spectral functions from tau decay

    SciTech Connect

    Dominguez, C. A.; Nasrallah, N. F.; Schilcher, K.

    2009-09-01

    The (nonstrange) vector and axial-vector spectral functions extracted from {tau} decay by the ALEPH Collaboration are confronted with QCD in the framework of a finite energy sum rule involving a polynomial kernel tuned to suppress the region beyond the kinematical end point where there is no longer data. This effectively allows for a QCD finite energy sum rule analysis to be performed beyond the region of the existing data. Results show excellent agreement between data and perturbative QCD in the remarkably wide energy range s=3-10 GeV{sup 2}, leaving room for a dimension d=4 vacuum condensate consistent with values in the literature. A hypothetical dimension d=2 term in the operator product expansion is found to be extremely small, consistent with zero. Fixed order and contour improved perturbation theory are used, with both leading to similar results within errors. Full consistency is found between vector and axial-vector channel results.

  3. 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).

  4. Search for second-class currents in tau;{-} --> omegapi;{-}nu_{tau}.

    PubMed

    Aubert, B; Karyotakis, Y; Lees, J P; Poireau, V; Prencipe, E; Prudent, X; Tisserand, V; Tico, J Garra; 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; Tackmann, K; Tanabe, T; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Asgeirsson, D J; Fulsom, B G; 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; Zhang, L; 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; 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; Wilson, R J; 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; Volk, A; 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; Chaisanguanthum, K S; Morii, M; Adametz, A; Marks, J; Schenk, S; Uwer, U; Bernlochner, F U; Klose, V; Lacker, H M; Bard, D J; 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; Béquilleux, J; D'Orazio, A; Davier, M; Derkach, D; da Costa, J Firmino; Grosdidier, G; Le Diberder, F; Lepeltier, V; Lutz, A M; Malaescu, B; Pruvot, S; 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; Saremi, S; 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; Lazzaro, A; Lombardo, V; Palombo, F; Stracka, S; Bauer, J M; Cremaldi, L; Godang, R; Kroeger, R; Sonnek, P; Summers, D J; Zhao, H W; 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; 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; 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; Pegna, D Lopes; 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; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Wilson, F F; Emery, S; Esteve, L; de Monchenault, G Hamel; Kozanecki, W; Vasseur, G; Yèche, Ch; Zito, M; Allen, M T; Aston, D; 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; Sevilla, M Franco; 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; Marsiske, H; Messner, R; Muller, D R; Neal, H; Nelson, S; O'Grady, C P; Ofte, I; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; West, C A; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Young, C C; Ziegler, V; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Burchat, P R; Edwards, A J; Miyashita, T S; Ahmed, S; Alam, M S; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Soffer, A; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Wray, B C; Drummond, B W; Izen, J M; Lou, X C; Bianchi, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Choi, H H F; Hamano, K; King, G J; Kowalewski, R; Lewczuk, M J; Nugent, I M; Roney, J M; Sobie, R J; Gershon, T J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Puccio, E M T; Band, H R; Chen, X; Dasu, S; Flood, K T; Pan, Y; Prepost, R; Vuosalo, C O; Wu, S L

    2009-07-24

    We report an analysis of tau;{-} decaying into omegapi;{-}nu_{tau} with omega --> pi;{+}pi;{-}pi;{0} using a data sample containing nearly 320 x 10;{6}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. PMID:19659341

  5. Measurement of the Tau Lepton Lifetime at Opal

    NASA Astrophysics Data System (ADS)

    Janissen, Anna Cornelia

    1993-01-01

    This thesis describes a new measurement of the tau (tau) lepton lifetime using two statistically independent techniques each associated with one of the two principle decay topologies of the tau to one and three charged particles, respectively. The measurement was performed with data collected in 1990 and 1991 at the OPAL detector at the LEP e^+e ^- colliding beam accelerator at CERN. The LEP collider operates at a significantly higher energy than previous e^+e^- colliders. This presents a new experimental opportunity to investigate the physics associated with the tau<=pton in general and the tau lifetime in particular. The tau lepton is one of three similar electron -like particles: e, mu, and tau. These leptons exhibit a hierarchy of masses with: m_{e} < m_ {mu} < m_{tau}. While the electron is stable, the mu and the tau are unstable and decay via the weak interaction charged current. It is a fundamental feature of the standard model of fundamental particles and their interactions that this weak charged current has exactly the same strength for each of the three leptons; a phenomenon called lepton universality. The tau lifetime, tau_tau, can be related to the mu lifetime, tau_ mu, and the average leptonic branching ratio, BR(tau to lnu| nu), by:tau_ tau = tau_mu {G_mu G_{e}over G_tau G_ l} ({m_muover m_tau})^5 {rm BR}(tautolnu|nu)R where R is a calculable factor to account for phase space and radiative corrections, and G _l is the Fermi effective coupling strength of the weak charged current to the lepton l. Lepton universality implies that G _mu = G_{e} = G_tau. The experimentally measured tau lifetime, together with the measurements of the other quantities in the above relation, can be interpreted as a direct test of lepton universality. The tau lifetime measured with each of the two independent techniques is: eqalign{tau_1 &rm= 296.4+/-7.1(stat.)+/- 3.8(sys.) fscr tau_3 &rm= 286.3+/-7.4(stat.)+/-5.2(sys.) fs.}The systematic uncertainties for each of the

  6. Search for neutral MSSM Higgs bosons decaying to tau(+)tau(-) pairs in proton-proton collisions root s=7 TeV with the ATLAS detector

    SciTech Connect

    Aad, G.; Abbott, B; Abdallah, J; Abdelalim, AA; Abdesselam, A; Abdinov, O; Abi, B; Abolins, M; Abramowicz, H; Abreu, H; Acerbi, E; Acharya, BS; Adams, DL; Addy, TN; Adelman, J; Aderholz, M; Adomeit, S; Adragna, P; Adye, T; Aefsky, S; Aguilar-Saavedra, JA

    2011-11-11

    A search for neutral Higgs bosons decaying to pairs of {tau} leptons with the ATLAS detector at the LHC is presented. The analysis is based on proton-proton collisions at a center-of-mass energy of 7 TeV, recorded in 2010 and corresponding to an integrated luminosity of 36 pb{sup -1}. After signal selection, 276 events are observed in this data sample. The observed number of events is consistent with the total expected background of 269 {+-} 36 events. Exclusion limits at the 95% confidence level are derived for the production cross section of a generic Higgs boson {phi} as a function of the Higgs boson mass and for A/H/h production in the Minimal Supersymmetric Standard Model (MSSM) as a function of the parameters m{sub A} and tan {beta}.

  7. 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.

  8. Search for a low-mass higgs boson in Upsilon(3S)-->gammaA(0), A(0)-->tau(+)tau(-) at BABAR.

    PubMed

    Aubert, B; Karyotakis, Y; Lees, J P; Poireau, V; Prencipe, E; Prudent, X; Tisserand, V; Tico, J Garra; 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; Tackmann, K; Tanabe, T; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Asgeirsson, D J; Fulsom, B G; 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; Wilson, R J; 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; Chaisanguanthum, K S; Morii, M; Adametz, A; Marks, J; Schenk, S; Uwer, U; Bernlochner, F U; Klose, V; Lacker, H M; Lueck, T; Volk, A; Bard, D J; 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; Béquilleux, J; D'Orazio, A; Davier, M; Derkach, D; da Costa, J Firmino; Grosdidier, G; Le Diberder, F; Lepeltier, V; Lutz, A M; Malaescu, B; Pruvot, S; 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; 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; 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; 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; Gioi, L Li; Mazzoni, M A; Morganti, S; Piredda, G; Renga, F; Voena, C; Ebert, M; Hartmann, T; Schröder, 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; Yèche, Ch; Zito, M; Allen, M T; Aston, D; 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; Sevilla, M Franco; 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; Marsiske, H; Messner, R; Muller, D R; Neal, H; Nelson, S; O'Grady, C P; Ofte, I; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; West, C A; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Young, C C; Ziegler, V; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Bellis, M; Burchat, P R; Edwards, A J; Miyashita, T S; Ahmed, S; Alam, M S; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Soffer, A; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Wray, B C; Drummond, B W; Izen, J M; Lou, X C; Bianchi, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Choi, H H F; Hamano, K; King, G J; Kowalewski, R; Lewczuk, M J; Nugent, I M; Roney, J M; Sobie, R J; Gershon, T J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Puccio, E M T; Band, H R; Chen, X; Dasu, S; Flood, K T; Pan, Y; Prepost, R; Vuosalo, C O; Wu, S L

    2009-10-30

    We search for a light Higgs boson A0 in the radiative decay Upsilon(3S)-->gammaA(0), A(0)-->tau+tau-, tau+-->e+nu(e)nu(tau), or tau+-->mu+nu(mu)nu(tau). The data sample contains 122x10(6) Upsilon(3S) events recorded with the BABAR detector. We find no evidence for a narrow structure in the studied tau+tau- invariant mass region of 4.03tau+tau-)<10.10 GeV/c2. We exclude at the 90% confidence level (C.L.) a low-mass Higgs boson decaying to tau+tau- with a product branching fraction B(Upsilon(3S)-->gammaA(0))xB(A(0)-->tau+tau-)>(1.5-16)x10(-5) across the m(tau+tau-) range. We also set a 90% C.L. upper limit on the tau+tau- decay of the eta(b) at B(eta(b)-->tau+tau-)<8%. PMID:19905799

  9. Can we see tau-Flavour Violation at the LHC?

    SciTech Connect

    Carquin, E.; Gomez, M. E.; Rodriguez-Quintero, J.

    2010-02-10

    We study the conditions required for chi{sub 2}->chi+tau{sup +}-mu{sup +}- decays to yield observable tau flavour violation at the LHC, for cosmologically interesting values of the neutralino relic density.

  10. 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).

  11. 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

  12. Neuronal activity enhances tau propagation and tau pathology in vivo.

    PubMed

    Wu, Jessica W; Hussaini, S Abid; Bastille, Isle M; Rodriguez, Gustavo A; Mrejeru, Ana; Rilett, Kelly; Sanders, David W; Cook, Casey; Fu, Hongjun; Boonen, Rick A C M; Herman, Mathieu; Nahmani, Eden; Emrani, Sheina; Figueroa, Y Helen; Diamond, Marc I; Clelland, Catherine L; Wray, Selina; Duff, Karen E

    2016-08-01

    Tau protein can transfer between neurons transneuronally and trans-synaptically, which is thought to explain the progressive spread of tauopathy observed in the brain of patients with Alzheimer's disease. Here we show that physiological tau released from donor cells can transfer to recipient cells via the medium, suggesting that at least one mechanism by which tau can transfer is via the extracellular space. Neuronal activity has been shown to regulate tau secretion, but its effect on tau pathology is unknown. Using optogenetic and chemogenetic approaches, we found that increased neuronal activity stimulates the release of tau in vitro and enhances tau pathology in vivo. These data have implications for disease pathogenesis and therapeutic strategies for Alzheimer's disease and other tauopathies. PMID:27322420

  13. 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.

  14. 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.

  15. 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.

  16. 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.

  17. 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 Aβ and intracellular neurofibrillary tangles composed of hyperphosphorylated tau proteins. According to the now well-accepted amyloid cascade hypothesis is the Aβ 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 Aβ 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

  18. W{right arrow} {tau} {nu} at the Tevatron

    SciTech Connect

    Serban Protopopescu

    1998-12-01

    We present results from the CDF and D0 detectors on the production of W-bosons decaying to {tau}{nu}{sub {tau}} at the FNAL Tevatron from data taken between 1992 and 1996. From CDF comes the first observation of W charge asymmetry in W {yields} {tau}{nu} final states, and from D0 a new measurement of g{sup W}{sub {tau}}/g{sup W}{sub e} , 1.003 {+-} 0.032.

  19. Improved limits on lepton-flavor-violating tau decays to lphi, lrho, lK, and lK.

    PubMed

    Aubert, B; Karyotakis, Y; Lees, J P; Poireau, V; Prencipe, E; Prudent, X; Tisserand, V; Tico, J Garra; 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; Tackmann, K; Tanabe, T; Hawkes, C M; Soni, N; Watson, A T; Koch, H; Schroeder, T; Asgeirsson, D J; Fulsom, B G; 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; Abachi, S; Buchanan, C; Atmacan, H; Gary, J W; Liu, F; Long, O; Vitug, G M; Yasin, Z; Zhang, L; 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; Winstrom, L O; Cheng, C H; Doll, D A; 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; Bloom, P C; Ford, W T; Gaz, A; Hirschauer, J F; Nagel, M; Nauenberg, U; Smith, J G; Wagner, S R; Ayad, R; Soffer, A; Toki, W H; Wilson, R J; 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; Volk, A; Bernard, D; Bonneaud, G R; 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; Chaisanguanthum, K S; Morii, M; Adametz, A; Marks, J; Schenk, S; Uwer, U; Bernlochner, F U; Klose, V; Lacker, H M; Bard, D J; 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; Béquilleux, J; D'Orazio, A; Davier, M; Derkach, D; Firmino da Costa, J; Grosdidier, G; Le Diberder, F; Lepeltier, V; Lutz, A M; Malaescu, B; Pruvot, S; 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; Saremi, S; 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; Lazzaro, A; Lombardo, V; Palombo, F; Stracka, S; Bauer, J M; Cremaldi, L; Godang, R; Kroeger, R; Summers, D J; Zhao, H W; 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; 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; 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; 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; Schröder, 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; Yèche, Ch; Zito, M; Allen, M T; Aston, D; 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; 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; Marsiske, H; Messner, R; Muller, D R; Neal, H; Nelson, S; O'Grady, C P; Ofte, I; Perl, M; Ratcliff, B N; Roodman, A; Salnikov, A A; Schindler, R H; Schwiening, J; Snyder, A; Su, D; Sullivan, M K; Suzuki, K; Swain, S K; Thompson, J M; Va'vra, J; Wagner, A P; Weaver, M; West, C A; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Yi, K; Young, C C; Ziegler, V; Chen, X R; Liu, H; Park, W; Purohit, M V; White, R M; Wilson, J R; Burchat, P R; Edwards, A J; Miyashita, T S; Ahmed, S; Alam, M S; Ernst, J A; Pan, B; Saeed, M A; Zain, S B; Spanier, S M; Wogsland, B J; Eckmann, R; Ritchie, J L; Ruland, A M; Schilling, C J; Schwitters, R F; Wray, B C; Drummond, B W; Izen, J M; Lou, X C; Bianchi, F; Gamba, D; Pelliccioni, M; Bomben, M; Bosisio, L; Cartaro, C; Della Ricca, G; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Milanes, D A; Oyanguren, A; Albert, J; Banerjee, Sw; Bhuyan, B; Choi, H H F; Hamano, K; King, G J; Kowalewski, R; Lewczuk, M J; Nugent, I M; Roney, J M; Sobie, R J; Gershon, T J; Harrison, P F; Ilic, J; Latham, T E; Mohanty, G B; Puccio, E M T; Band, H R; Chen, X; Dasu, S; Flood, K T; Pan, Y; Prepost, R; Vuosalo, C O; Wu, S L

    2009-07-10

    We search for the neutrinoless, lepton-flavor-violating tau decays tau- -->l-}V0, where l is an electron or muon and V0 is a vector meson reconstructed as phi-->K+K-, rho-->pi+pi-, K-->K+pi-, K[over ]-->K-pi+. The analysis has been performed using 451 fb-1 of data collected at an e+e- 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)x10-8 at the 90% confidence level. PMID:19659196

  20. 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.

  1. 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.

  2. Tau imaging in neurodegenerative diseases.

    PubMed

    Dani, M; Brooks, D J; Edison, P

    2016-06-01

    Aggregated tau protein is a major neuropathological substrate central to the pathophysiology of neurodegenerative diseases such as Alzheimer's disease (AD), frontotemporal dementia, progressive supranuclear palsy, corticobasal degeneration and chronic traumatic encephalopathy. In AD, it has been shown that the density of hyperphosphorylated tau tangles correlates closely with neuronal dysfunction and cell death, unlike β-amyloid. Until now, diagnostic and pathologic information about tau deposition has only been available from invasive techniques such as brain biopsy or autopsy. The recent development of selective in-vivo tau PET imaging ligands including [(18)F]THK523, [(18)F]THK5117, [(18)F]THK5105 and [(18)F]THK5351, [(18)F]AV1451(T807) and [(11)C]PBB3 has provided information about the role of tau in the early phases of neurodegenerative diseases, and provided support for diagnosis, prognosis, and imaging biomarkers to track disease progression. Moreover, the spatial and longitudinal relationship of tau distribution compared with β - amyloid and other pathologies in these diseases can be mapped. In this review, we discuss the role of aggregated tau in tauopathies, the challenges posed in developing selective tau ligands as biomarkers, the state of development in tau tracers, and the new clinical information that has been uncovered, as well as the opportunities for improving diagnosis and designing clinical trials in the future. PMID:26572762

  3. Tau physics at future facilities

    SciTech Connect

    Perl, M.L.

    1994-12-01

    This paper dicusses and projects the tau research which may be carried out at CESR, at BEPC, at the SLC, in the next few years at LEP I, at the asymmetric B-factories under construction in Japan and the United States and, if built, a tau-charm factory. As the size of tau data sets increases, there is an increasing need to reduce the effects of systematic errors on the precision and search range of experiments. In most areas of tau physics there is a large amount of progress to be made, but in a few areas it will be difficult to substantially improve the precision of present measurements.

  4. Effects of tau domain-specific antibodies and intravenous immunoglobulin on tau aggregation and aggregate degradation.

    PubMed

    Esteves-Villanueva, Jose O; Trzeciakiewicz, Hanna; Loeffler, David A; Martić, Sanela

    2015-01-20

    Tau pathology, including neurofibrillary tangles, develops in Alzheimer's disease (AD). The aggregation and hyperphosphorylation of tau are potential therapeutic targets for AD. Administration of anti-tau antibodies reduces tau pathology in transgenic "tauopathy" mice; however, the optimal tau epitopes and conformations to target are unclear. Also unknown is whether intravenous immunoglobulin (IVIG) products, currently being evaluated in AD trials, exert effects on pathological tau. This study examined the effects of anti-tau antibodies targeting different tau epitopes and the IVIG Gammagard on tau aggregation and preformed tau aggregates. Tau aggregation was assessed by transmission electron microscopy and fluorescence spectroscopy, and the binding affinity of the anti-tau antibodies for tau was evaluated by enzyme-linked immunosorbent assays. Antibodies used were anti-tau 1-150 ("D-8"), anti-tau 259-266 ("Paired-262"), anti-tau 341-360 ("A-10"), and anti-tau 404-441 ("Tau-46"), which bind to tau's N-terminus, microtubule binding domain (MBD) repeat sequences R1 and R4, and the C-terminus, respectively. The antibodies Paired-262 and A-10, but not D-8 and Tau-46, reduced tau fibrillization and degraded preformed tau aggregates, whereas the IVIG reduced tau aggregation but did not alter preformed aggregates. The binding affinities of the antibodies for the epitope for which they were specific did not appear to be related to their effects on tau aggregation. These results confirm that antibody binding to tau's MBD repeat sequences may inhibit tau aggregation and indicate that such antibodies may also degrade preformed tau aggregates. In the presence of anti-tau antibodies, the resulting tau morphologies were antigen-dependent. The results also suggested the possibility of different pathways regulating antibody-mediated inhibition of tau aggregation and antibody-mediated degradation of preformed tau aggregates. PMID:25545358

  5. Observation of B{sup +{yields}}D*{sup 0{tau}+{nu}}{sub {tau}}and evidence for B{sup +{yields}}D{sup 0{tau}+{nu}}{sub {tau}}at Belle

    SciTech Connect

    Bozek, A.; Rozanska, M.; Kapusta, P.; Matyja, A.; Ostrowicz, W.; Stypula, J.; Adachi, I.; Higuchi, T.; Iwasaki, Y.; Kichimi, H.; Krokovny, P.; Nakao, M.; Nishida, S.; Nozaki, T.; Sakai, Y.; Schuemann, J.; Trabelsi, K.; Uehara, S.; Uno, S.; Aihara, H.

    2010-10-01

    We present measurements of B{sup +{yields}}D*{sup 0{tau}+{nu}}{sub {tau}}and B{sup +{yields}}D{sup 0{tau}+{nu}}{sub {tau}}decays in a data sample of 657x10{sup 6} BB pairs collected with the Belle detector at the KEKB asymmetric-energy e{sup +}e{sup -} collider. We find 446{sub -56}{sup +58} B{sup +{yields}}D*{sup 0{tau}+{nu}}{sub {tau}}events with a significance of 8.1 standard deviations, and 146{sub -41}{sup +42} B{sup +{yields}}D{sup 0{tau}+{nu}}{sub {tau}}events with a significance of 3.5 standard deviations. The latter signal provides the first evidence for this decay mode. The measured branching fractions are B(B{sup +{yields}}D*{sup 0{tau}+{nu}}{sub {tau}})=(2.12{sub -0.27}{sup +0.28}(stat){+-}0.29(syst))% and B(B{sup +{yields}}D{sup 0{tau}+{nu}}{sub {tau}})=(0.77{+-}0.22(stat){+-}0.12(syst))%.

  6. 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.

  7. Search for the Higgs Boson Decaying to Two Tau Leptons in $p\\bar{p}$ Collisions at a Center of Mass Energy of 1.96 Tev

    SciTech Connect

    Elagin, Andrey Lvovich

    2011-12-01

    A search for the Higgs boson decaying to $\\tau\\tau$ using 7.8~fb$^{-1}$ of $p\\bar{p}$ collisions at 1.96~TeV collected with CDF II detector is presented. The search is sensitive to four production mechanisms of the Higgs boson: ggH, WH, ZH and VBF. Modes where one tau decay leptonically, and another decay, hadronically, are considered. Two novel techniques are developed and used in the search. A Probabilistic Particle Flow Algorithm is used for energy measurements of the hadronic tau candidates. The signal is discriminated from backgrounds by the Missing Mass Calculator, which allows for full invariant mass reconstruction of $\\tau\\tau$ pair. The data are found to be consistent with the background only hypothesis. Therefore a 95\\% confidence level upper limit on the Standard Model Higgs boson cross section was set. At $M_H$$=$120~GeV/$c^2$ observed limit is 14.9$\\times\\sigma_{SM}\\times Br (H → ττ)$.

  8. 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.

  9. Measurement of the pseudoscalar decay constant f{sub D{sub s}} using D{sub s}{sup +}{yields}{tau}{sup +}{nu}, {tau}{sup +}{yields}{rho}{sup +}{nu} decays

    SciTech Connect

    Naik, P.; Rademacker, J.; Asner, D. M.; Edwards, K. W.; Randrianarivony, K.; Reed, J.; Robichaud, A. N.; Tatishvili, G.; White, E. J.; Briere, R. A.; Vogel, H.; Onyisi, P. U. E.; Rosner, J. L.; Alexander, J. P.; Cassel, D. G.; Ehrlich, R.; Fields, L.; Gibbons, L.; Gray, S. W.; Hartill, D. L.

    2009-12-01

    Analyzing 600 pb{sup -1} of e{sup +}e{sup -} collisions at 4170 MeV center-of-mass energy with the CLEO-c detector, we measure the branching fraction B(D{sub s}{sup +}{yields}{tau}{sup +}{nu})=(5.52{+-}0.57{+-}0.21)% using the {tau}{sup +}{yields}{rho}{sup +}{nu} decay mode. Combining with other CLEO measurements of B(D{sub s}{sup +}{yields}{tau}{sup +}{nu}) we determine the pseudoscalar decay constant f{sub D{sub s}}=(259.7{+-}7.8{+-}3.4) MeV consistent with the value obtained from our D{sub s}{sup +}{yields}{mu}{sup +}{nu} measurement of (257.6{+-}10.3{+-}4.3) MeV. Combining these measurements we find a value of f{sub D{sub s}}=(259.0{+-}6.2{+-}3.0) MeV, that differs from the most accurate prediction based on unquenched lattice gauge theory of (241{+-}3) MeV by 2.4 standard deviations. We also present the first measurements of B(D{sub s}{sup +}{yields}K{sup 0}{pi}{sup +}{pi}{sup 0})=(1.00{+-}0.18{+-}0.04)%, and B(D{sub s}{sup +}{yields}{pi}{sup +}{pi}{sup 0}{pi}{sup 0})=(0.65{+-}0.13{+-}0.03)%, and measure a new value for B(D{sub s}{sup +}{yields}{eta}{rho}{sup +})=(8.9{+-}0.6{+-}0.5)%.

  10. Is there a paradox in CP asymmetries of {tau}{sup {+-}}{yields}K{sub L,S}{pi}{sup {+-}}{nu} decays?

    SciTech Connect

    Calderon, G.; Delepine, D.; Castro, G. Lopez

    2007-04-01

    Based on the description of unstable K{sub L,S} particles in quantum field theory (QFT), we compute the time-dependent probabilities for transitions between asymptotic states in {tau}{sup {+-}}{yields}[{pi}{sup +}{pi}{sup -}]{sub K}{pi}{sup {+-}}{nu} decays, where the pair [{pi}{sup +}{pi}{sup -}]{sub K} is the product of (intermediate state) neutral kaon decays. Then we propose a definition of {tau} decays into K{sub L} and K{sub S} states, which reflects into the cancellation between their CP rate asymmetries, thus solving in a natural way the paradox pointed out in [I. I. Bigi and A. I. Sanda, Phys. Lett. B 625, 47 (2005).]. Since our definition of K{sub L,S} final states in {tau} decays is motivated on experimental grounds, our predictions for the integrated CP rate asymmetries can be tested in a dedicated experiment.

  11. 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; Höcker, 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; Côté, 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; Chauveau, J; David, P; Del Buono, L; de la Vaissière, Ch; Hamon, O; Hartfiel, B L; Leruste, Ph; Malclès, J; Ocariz, J; Roos, L; Therin, G; Gladney, L; Biasini, M; Covarelli, R; Angelini, C; Batignani, G; Bettarini, S; Bucci, F; Calderini, G; Carpinelli, M; Cenci, R; Forti, F; Giorgi, M A; Lusiani, A; Marchiori, G; Mazur, M A; Morganti, M; Neri, N; Paoloni, E; Rizzo, G; Walsh, J 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; Del Re, D; 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; Ebert, M; Schröder, H; Waldi, R; Adye, T; Franek, B; Olaiya, E O; Ricciardi, S; Wilson, F F; Aleksan, R; Emery, S; Gaidot, A; Ganzhur, S F; Hamel de Monchenault, G; Kozanecki, W; Legendre, M; Vasseur, G; Yèche, Ch; Zito, M; Chen, X R; Liu, H; Park, W; Purohit, M V; Wilson, J R; Allen, M T; Aston, D; Bartoldus, R; Bechtle, P; Berger, N; Claus, R; Coleman, J P; Convery, M R; Dingfelder, J C; Dorfan, J; Dubois-Felsmann, G P; Dujmic, D; Dunwoodie, W; Field, R C; Glanzman, T; Gowdy, S J; Graham, M T; Grenier, P; Halyo, V; Hast, C; Hryn'ova, T; Innes, W R; Kelsey, M H; Kim, P; Leith, D W G S; Li, S; Luitz, S; Luth, V; Lynch, H L; MacFarlane, D B; Marsiske, H; Messner, R; Muller, D R; O'Grady, C P; Ozcan, V E; Perazzo, A; Perl, M; Pulliam, T; 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; Wagner, A P; Weaver, M; Weinstein, A J R; Wisniewski, W J; Wittgen, M; Wright, D H; Wulsin, H W; Yarritu, A K; Yi, K; Young, C C; Burchat, P R; Edwards, A J; Majewski, S A; Petersen, B A; Wilden, L; Ahmed, S; Alam, M S; Bula, R; Ernst, J A; Jain, V; Pan, B; Saeed, M A; Wappler, F R; Zain, S B; Bugg, W; Krishnamurthy, M; Spanier, S M; Eckmann, R; Ritchie, J L; Satpathy, A; Schilling, C J; Schwitters, R F; Izen, J M; Lou, X C; Ye, S; Bianchi, F; Gallo, F; Gamba, D; Bomben, M; Bosisio, L; Cartaro, C; Cossutti, F; Della Ricca, G; Dittongo, S; Lanceri, L; Vitale, L; Azzolini, V; Lopez-March, N; Martinez-Vidal, F; Banerjee, Sw; Bhuyan, B; Brown, C M; Fortin, D; Hamano, K; Kowalewski, R; Nugent, I M; Roney, J M; Sobie, R J; Back, J J; Harrison, P F; Latham, T E; Mohanty, G B; Pappagallo, M; Band, H R; Chen, X; Cheng, B; Dasu, S; Datta, M; Flood, K T; Hollar, J J; Kutter, P E; Mellado, B; Mihalyi, A; Pan, Y; Pierini, M; Prepost, R; Wu, S L; Yu, Z; Neal, 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

  12. The Tau-Charm Factory and tau physics

    SciTech Connect

    Perl, M.L.

    1989-04-01

    An international group of physicists is developing the concept and design of a Tau-Charm Factory: a two-ring, electron-positron, circular collider with 1.5 /< =/ /radical/s /< =/ 4.2 GeV and a design luminosity of 10/sup 33/ cm/sup /minus/2/ s/sup /minus/1/. This paper presents the concept of the facility and outlines the tau lepton physics which can be done. A companion talk by R. Schindler discusses the D/sup 0/, D/sup /+-//, and D/sub s/ physics at a Tau-Charm Factory. 25 refs., 2 tabs.

  13. Tau exon 10 alternative splicing and tauopathies

    PubMed Central

    Liu, Fei; Gong, Cheng-Xin

    2008-01-01

    Abnormalities of microtubule-associated protein tau play a central role in neurofibrillary degeneration in several neurodegenerative disorders that collectively called tauopathies. Six isoforms of tau are expressed in adult human brain, which result from alternative splicing of pre-mRNA generated from a single tau gene. Alternative splicing of tau exon 10 results in tau isoforms containing either three or four microtubule-binding repeats (3R-tau and 4R-tau, respectively). Approximately equal levels of 3R-tau and 4R-tau are expressed in normal adult human brain, but the 3R-tau/4R-tau ratio is altered in the brains in several tauopathies. Discovery of silence mutations and intronic mutations of tau gene in some individuals with frontotemporal dementia with Parkinsonism linked to chromosome 17 (FTDP-17), which only disrupt tau exon 10 splicing but do not alter tau's primary sequence, demonstrates that dysregulation of tau exon 10 alternative splicing and consequently of 3R-tau/4R-tau balance is sufficient to cause neurodegeneration and dementia. Here, we review the gene structure, transcripts and protein isoforms of tau, followed by the regulation of exon 10 splicing that determines the expression of 3R-tau or 4R-tau. Finally, dysregulation of exon 10 splicing of tau in several tauopathies is discussed. Understanding the molecular mechanisms by which tau exon 10 splicing is regulated and how it is disrupted in tauopathies will provide new insight into the mechanisms of these tauopathies and help identify new therapeutic targets to treat these disorders. PMID:18616804

  14. 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.

  15. 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.

  16. 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

  17. 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

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

    PubMed

    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

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

    PubMed Central

    Ando, Kunie; Leroy, Karelle; Héraud, Céline; Yilmaz, Zehra; Authelet, Michèle; Suain, Valèrie; 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

  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. 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.

  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. 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.

  4. 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.

  5. 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; Erö, J; Fabjan, C; Friedl, M; Frühwirth, R; Ghete, V M; Hammer, J; Hänsel, S; Hoch, M; Hörmann, N; Hrubec, J; Jeitler, M; Kasieczka, G; Kiesenhofer, W; Krammer, M; Liko, D; Mikulec, I; Pernicka, M; Rohringer, H; Schöfbeck, 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; Grégoire, 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; Müntel, M; Raidal, M; Rebane, L; Azzolini, V; Eerola, P; Fedi, G; Czellar, S; Härkönen, J; Heikkinen, A; Karimäki, V; Kinnunen, R; Kortelainen, M J; Lampén, T; Lassila-Perini, K; Lehti, S; Lindén, T; Luukka, P; Mäenpää, 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; Miné, 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; Gelé, 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; Flügge, 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

  6. 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

  7. 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.

  8. 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.}

  9. 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.

  10. 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

  11. Interaction of tau with the RNA-Binding Protein TIA1 Regulates tau Pathophysiology and Toxicity.

    PubMed

    Vanderweyde, Tara; Apicco, Daniel J; Youmans-Kidder, Katherine; Ash, Peter E A; Cook, Casey; Lummertz da Rocha, Edroaldo; Jansen-West, Karen; Frame, Alissa A; Citro, Allison; Leszyk, John D; Ivanov, Pavel; Abisambra, Jose F; Steffen, Martin; Li, Hu; Petrucelli, Leonard; Wolozin, Benjamin

    2016-05-17

    Dendritic mislocalization of microtubule associated protein tau is a hallmark of tauopathies, but the role of dendritic tau is unknown. We now report that tau interacts with the RNA-binding protein (RBP) TIA1 in brain tissue, and we present the brain-protein interactome network for TIA1. Analysis of the TIA1 interactome in brain tissue from wild-type (WT) and tau knockout mice demonstrates that tau is required for normal interactions of TIA1 with proteins linked to RNA metabolism, including ribosomal proteins and RBPs. Expression studies show that tau regulates the distribution of TIA1, and tau accelerates stress granule (SG) formation. Conversely, TIA1 knockdown or knockout inhibits tau misfolding and associated toxicity in cultured hippocampal neurons, while overexpressing TIA1 induces tau misfolding and stimulates neurodegeneration. Pharmacological interventions that prevent SG formation also inhibit tau pathophysiology. These studies suggest that the pathophysiology of tauopathy requires an intimate interaction with RNA-binding proteins. PMID:27160897

  12. A Tau-Charm Factory at CEBAF

    SciTech Connect

    Seth, K.K.

    1994-04-01

    It is proposed that a Tau Charm Factory represents a natural extension of CEBAF into higher energy domains. The exciting nature of the physics of charm quarks and tau leptons is briefly reviewed and it is suggested that the concept of a linac-ring collider as a Tau Charm Factory at CEBAF should be seriously studied.

  13. 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 \

  14. Tau identification at D0

    SciTech Connect

    Galea, Cristina; /Radboud U. Nijmegen

    2006-12-01

    We describe methods to identify {tau} leptons produced in high energy p{bar p} collisions ({radical}s = 1.96 GeV) at the Tevatron, using the D0 detector. Different procedures used for discrimination against background particles misidentified as taus are also discussed. Finally, we present some physics results obtained by applying these methods to illustrate their performance.

  15. Searching for τ → μ γ lepton-flavor-violating decay at super Charm-Tau factory

    NASA Astrophysics Data System (ADS)

    Zhou, Hao; Zhang, Ren-You; Han, Liang; Ma, Wen-Gan; Guo, Lei; Chen, Chong

    2016-08-01

    We investigate the possibility of searching the lepton-flavor-violating (LFV) τ → μ γ rare decay at the Super Charm-Tau Factory (CTF). By comparing the kinematic distributions of the LFV signal and the standard model background, we develop an optimized event selection criterion which can significantly reduce the background events. It is concluded that the new 2 σ upper limit of about 1.9 × 10^{-9} on Br(τ → μ γ ) can be obtained at the CTF, which is beyond the capability of Super-B factory in searching τ lepton rare decay. Within the framework of the scalar leptoquark model, a joint constraint on λ _1 λ _2 and M_{LQ} can be derived from the upper bound on Br(τ → μ γ ). With 1000 fb^{-1} data expected at the CTF, we get λ _1λ _2 < 7.2 × 10^{-2} (M_{LQ} = 800 GeV) and M_{LQ} > 900 GeV (λ _1 λ _2 = 9 × 10^{-2}) at 95 % confidence level.

  16. 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.

  17. 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. /more authors..

    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}.

  18. 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.; /more authors..

    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.

  19. 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.

  20. 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

  1. 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.

  2. 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 González, 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; González, 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; Martínez, M; Martínez-Ballarín, 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; Mülmenstädt, 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; Palencia, E; Papadimitriou, V; Papaikonomou, A; Paramonov, A A; Parks, B; Pashapour, S; Patrick, J; Pauletta, G; Paulini, M; Paus, C; Peiffer, T; Pellett, D E; Penzo, A; Phillips, T J; Piacentino, G; Pianori, E; Pinera, L; Pitts, K; Plager, C; Pondrom, L; Poukhov, O; Pounder, N; Prakoshyn, F; Pronko, A; Proudfoot, J; Ptohos, F; Pueschel, E; Punzi, G; Pursley, J; Rademacker, J; Rahaman, A; Ramakrishnan, V; Ranjan, N; Redondo, I; Renton, P; Renz, M; Rescigno, M; Richter, S; Rimondi, F; Ristori, L; Robson, A; Rodrigo, T; Rodriguez, T; Rogers, E; Rolli, S; Roser, R; Rossi, M; Rossin, R; Roy, P; Ruiz, A; Russ, J; Rusu, V; Rutherford, B; Saarikko, H; Safonov, A; Sakumoto, W K; Saltó, O; Santi, L; Sarkar, S; Sartori, L; Sato, K; Savoy-Navarro, A; Schlabach, P; Schmidt, A; Schmidt, E E; Schmidt, M A; Schmidt, M P; Schmitt, M; Schwarz, T; Scodellaro, L; Scribano, A; Scuri, F; Sedov, A; Seidel, S; Seiya, Y; Semenov, A; Sexton-Kennedy, L; Sforza, F; Sfyrla, A; Shalhout, S Z; Shears, T; Shepard, P F; Shimojima, M; Shiraishi, S; Shochet, M; Shon, Y; Shreyber, I; Sinervo, P; Sisakyan, A; Slaughter, A J; Slaunwhite, J; Sliwa, K; Smith, J R; Snider, F D; Snihur, R; Soha, A; Somalwar, S; Sorin, V; Spreitzer, T; Squillacioti, P; Stanitzki, M; St Denis, R; Stelzer, B; Stelzer-Chilton, O; Stentz, D; Strologas, J; Strycker, G L; Suh, J S; Sukhanov, A; Suslov, I; Suzuki, T; Taffard, A; Takashima, R; Takeuchi, Y; Tanaka, R; Tecchio, M; Teng, P K; Terashi, K; Thom, J; Thompson, A S; Thompson, G A; Thomson, E; Tipton, P; Ttito-Guzmán, P; Tkaczyk, S; Toback, D; Tokar, S; Tollefson, K; Tomura, T; Tonelli, D; Torre, S; Torretta, D; Totaro, P; Tourneur, S; Trovato, M; Tsai, S-Y; Tu, Y; Turini, N; Ukegawa, F; Vallecorsa, S; van Remortel, N; Varganov, A; Vataga, E; Vázquez, F; Velev, G; Vellidis, C; Vidal, M; Vidal, R; Vila, I; Vilar, R; Vine, T; Vogel, M; Volobouev, I; Volpi, G; Wagner, P; Wagner, R G; Wagner, R L; Wagner, W; Wagner-Kuhr, J; Wakisaka, T; Wallny, R; Wang, S M; Warburton, A; Waters, D; Weinberger, M; Weinelt, J; Wester, W C; Whitehouse, B; Whiteson, D; Wicklund, A B; Wicklund, E; Wilbur, S; Williams, G; Williams, H H; Wilson, P; Winer, B L; Wittich, P; Wolbers, S; Wolfe, C; Wright, T; Wu, X; Würthwein, F; Xie, S; Yagil, A; Yamamoto, K; Yamaoka, J; Yang, U K; Yang, Y C; Yao, W M; Yeh, G P; Yi, K; Yoh, J; Yorita, K; Yoshida, T; Yu, G B; Yu, I; Yu, S S; Yun, J C; Zanello, L; Zanetti, A; Zhang, X; Zheng, Y; Zucchelli, S

    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

  3. Extracellular Monomeric Tau Protein Is Sufficient to Initiate the Spread of Tau Protein Pathology*

    PubMed Central

    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.

    2014-01-01

    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

  4. 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.

  5. 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

  6. 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}.

  7. Voyager observations of Zeta Tau

    NASA Technical Reports Server (NTRS)

    Carone, T. E.; Polidan, R. S.

    1987-01-01

    Two Voyager observations of Zeta Tau, a well-known Be/shell star of spectral type B1 IVe and vsin(i) = 220 km/s, separated by 503 days are presented and discussed. The observations show that in the spectral region shortward of Lyman-alpha, the 950-1150 A flux increased by about 40 percent, while in the region longward of 1300 A the flux increased by about 30 percent. Changes in features at 975 A and at 1020 A also appear. The observed change in the continuum flux is probably associated with a change in the effective temperature of the underlying B star, though change in the ubiquitous Fe II lines cannot be ruled out as the cause. The line variations are consistent with IUE spectra of Zeta Tau taken during the same time period.

  8. 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}.

  9. Improved measurement of absolute branching fraction of D{sub s}{sup +}{yields}{tau}{sup +}{nu}{sub {tau}}

    SciTech Connect

    Onyisi, P. U. E.; Rosner, J. L.; Alexander, J. P.; Cassel, D. G.; Duboscq, J. E.; Ehrlich, R.; Fields, L.; Galik, R. S.; Gibbons, L.; Gray, R.; Gray, S. W.; Hartill, D. L.; Heltsley, B. K.; Hertz, D.; Hunt, J. M.; Kandaswamy, J.; Kreinick, D. L.; Kuznetsov, V. E.; Ledoux, J.; Mahlke-Krueger, H.

    2009-03-01

    We have studied the leptonic decay D{sub s}{sup +}{yields}{tau}{sup +}{nu}{sub {tau}}, via the decay channel {tau}{sup +}{yields}e{sup +}{nu}{sub e}{nu}{sub {tau}}, using a sample of tagged D{sub s}{sup +} decays collected near the D{sub s}*{sup {+-}}D{sub s}{sup {+-}} peak production energy in e{sup +}e{sup -} collisions with the CLEO-c detector. We obtain B(D{sub s}{sup +}{yields}{tau}{sup +}{nu}{sub {tau}})=(5.30{+-}0.47{+-}0.22)% and determine the decay constant f{sub D{sub s}}=(252.5{+-}11.1{+-}5.2) MeV, where the first uncertainties are statistical and the second are systematic.

  10. Reduced CSF p-Tau181 to Tau ratio is a biomarker for FTLD-TDP

    PubMed Central

    Watts, Kelly; Grossman, Murray; Glass, Jonathan; Lah, James J.; Hales, Chadwick; Shelnutt, Matthew; Van Deerlin, Vivianna; Trojanowski, John Q.; Levey, Allan I.

    2013-01-01

    Objectives: To validate the ability of candidate CSF biomarkers to distinguish between the 2 main forms of frontotemporal lobar degeneration (FTLD), FTLD with TAR DNA-binding protein 43 (TDP-43) inclusions (FTLD-TDP) and FTLD with Tau inclusions (FTLD-Tau). Methods: Antemortem CSF samples were collected from 30 patients with FTLD in a single-center validation cohort, and CSF levels of 5 putative FTLD-TDP biomarkers as well as levels of total Tau (t-Tau) and Tau phosphorylated at threonine 181 (p-Tau181) were measured using independent assays. Biomarkers most associated with FTLD-TDP were then tested in a separate 2-center validation cohort composed of subjects with FTLD-TDP, FTLD-Tau, Alzheimer disease (AD), and cognitively normal subjects. The sensitivity and specificity of FTLD-TDP biomarkers were determined. Results: In the first validation cohort, FTLD-TDP cases had decreased levels of p-Tau181 and interleukin-23, and increased Fas. Reduced ratio of p-Tau181 to t-Tau (p/t-Tau) was the strongest predictor of FTLD-TDP pathology. Analysis in the second validation cohort showed CSF p/t-Tau ratio <0.37 to distinguish FTLD-TDP from FTLD-Tau, AD, and healthy seniors with 82% sensitivity and 82% specificity. Conclusion: A reduced CSF p/t-Tau ratio represents a reproducible, validated biomarker for FTLD-TDP with performance approaching well-established CSF AD biomarkers. Introducing this biomarker into research and the clinical arena can significantly increase the power of clinical trials targeting abnormal accumulations of TDP-43 or Tau, and select the appropriate patients for target-specific therapies. Classification of evidence: This study provides Class II evidence that the CSF p/t-Tau ratio distinguishes FTLD-TDP from FTLD-Tau. PMID:24174584

  11. 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

  12. Search for neutral Higgs bosons decaying to tau pairs in pp[over ] collisions at sqrt[s]=1.96 TeV.

    PubMed

    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; Anzelc, M S; Arnoud, Y; Arov, M; Askew, A; Asman, B; Assis Jesus, A C S; Atramentov, O; Autermann, C; Avila, C; Ay, C; Badaud, F; Baden, A; Bagby, L; Baldin, B; Bandurin, D V; Banerjee, P; Banerjee, S; Barberis, E; Bargassa, P; Baringer, P; Barnes, C; Barreto, J; Bartlett, J F; Bassler, U; Bauer, D; Bean, A; Begalli, M; Begel, M; Belanger-Champagne, C; Bellantoni, L; Bellavance, A; Benitez, J A; Beri, S B; Bernardi, G; Bernhard, R; Berntzon, L; Bertram, I; Besançon, M; Beuselinck, R; Bezzubov, V A; Bhat, P C; Bhatnagar, V; Binder, M; Biscarat, C; Black, K M; Blackler, I; Blazey, G; Blekman, F; Blessing, S; Bloch, D; Bloom, K; Blumenschein, U; Boehnlein, A; Boeriu, O; Bolton, T A; Borcherding, F; Borissov, G; Bos, K; Bose, T; Brandt, A; Brock, R; Brooijmans, G; Bross, A; Brown, D; Buchanan, N J; Buchholz, D; Buehler, M; Buescher, V; Burdin, S; Burke, S; Burnett, T H; Busato, E; Buszello, C P; Butler, J M; Calfayan, P; Calvet, S; Cammin, J; Caron, S; Carvalho, W; Casey, B C K; Cason, N M; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K M; Chandra, A; Chapin, D; Charles, F; Cheu, E; Chevallier, F; Cho, D K; Choi, S; Choudhary, B; Christofek, L; Claes, D; Clément, B; Clément, C; Coadou, Y; Cooke, M; Cooper, W E; Coppage, D; Corcoran, M; Cousinou, M-C; Cox, B; Crépé-Renaudin, S; Cutts, D; Cwiok, M; da Motta, H; Das, A; Das, M; Davies, B; Davies, G; Davis, G A; De, K; de Jong, P; de Jong, S J; De La Cruz-Burelo, E; De Oliveira Martins, C; Degenhardt, J D; Déliot, F; Demarteau, M; Demina, R; Demine, P; Denisov, D; Denisov, S P; Desai, S; Diehl, H T; Diesburg, M; Doidge, M; Dominguez, A; Dong, H; Dudko, L V; Duflot, L; Dugad, S R; Duperrin, A; Dyer, J; Dyshkant, A; Eads, M; Edmunds, D; Edwards, T; Ellison, J; Elmsheuser, J; Elvira, V D; Eno, S; Ermolov, P; Estrada, J; Evans, H; Evdokimov, A; Evdokimov, V N; Fatakia, S N; Feligioni, L; Ferapontov, A V; Ferbel, T; Fiedler, F; Filthaut, F; Fisher, W; Fisk, H E; Fleck, I; Ford, M; Fortner, M; Fox, H; Fu, S; Fuess, S; Gadfort, T; Galea, C F; Gallas, E; Galyaev, E; Garcia, C; Garcia-Bellido, A; Gardner, J; Gavrilov, V; Gay, A; Gay, P; Gelé, D; Gelhaus, R; Gerber, C E; Gershtein, Y; Gillberg, D; Ginther, G; Gollub, N; Gómez, B; Gounder, K; Goussiou, A; Grannis, P D; Greenlee, H; Greenwood, Z D; Gregores, E M; Grenier, G; Gris, Ph; Grivaz, J-F; 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; Hanagaki, K; Harder, K; Harel, A; Harrington, R; Hauptman, J M; Hauser, R; Hays, J; Hebbeker, T; Hedin, D; Hegeman, J G; Heinmiller, J M; Heinson, A P; Heintz, U; Hensel, C; Hesketh, G; Hildreth, M D; Hirosky, R; Hobbs, J D; Hoeneisen, B; Hoeth, H; Hohlfeld, M; Hong, S J; Hooper, R; 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; Jenkins, A; Jesik, R; Johns, K; Johnson, C; Johnson, M; Jonckheere, A; Jonsson, P; Juste, A; Käfer, D; Kahn, S; Kajfasz, E; Kalinin, A M; Kalk, J M; Kalk, J R; Kappler, S; Karmanov, D; Kasper, J; Kasper, P; Katsanos, I; Kau, D; Kaur, R; Kehoe, R; Kermiche, S; Kesisoglou, S; Khalatyan, N; Khanov, A; Kharchilava, A; Kharzheev, Y M; Khatidze, D; Kim, H; Kim, T J; Kirby, M H; Klima, B; Kohli, J M; Konrath, J-P; Kopal, M; Korablev, V M; Kotcher, J; Kothari, B; Koubarovsky, A; Kozelov, A V; Kozminski, J; Kryemadhi, A; Krzywdzinski, S; Kuhl, T; Kumar, A; Kunori, S; Kupco, A; Kurca, T; Kvita, J; Lager, S; Lammers, S; Landsberg, G; Lazoflores, J; Le Bihan, A-C; Lebrun, P; Lee, W M; Leflat, A; Lehner, F; Lesne, V; Leveque, J; Lewis, P; Li, J; Li, Q Z; Lima, J G R; Lincoln, D; Linnemann, J; Lipaev, V V; Lipton, R; Liu, Z; Lobo, L; Lobodenko, A; Lokajicek, M; Lounis, A; Love, P; Lubatti, H J; Lynker, M; Lyon, A L; Maciel, A K A; Madaras, R J; Mättig, P; Magass, C; Magerkurth, A; Magnan, A-M; Makovec, N; Mal, P K; Malbouisson, H B; Malik, S; Malyshev, V L; Mao, H S; Maravin, Y; Martens, M; Mattingly, S E K; McCarthy, R; McCroskey, R; Meder, D; Melnitchouk, A; Mendes, A; Mendoza, L; Merkin, M; Merritt, K W; Meyer, A; Meyer, J; Michaut, M; Miettinen, H; Millet, T; Mitrevski, J; Molina, J; Mondal, N K; Monk, J; Moore, R W; Moulik, T; Muanza, G S; Mulders, M; Mulhearn, M; Mundim, L; Mutaf, Y D; Nagy, E; Naimuddin, M; Narain, M; Naumann, N A; Neal, H A; Negret, J P; Nelson, S; Neustroev, P; Noeding, C; Nomerotski, A; Novaes, S F; Nunnemann, T; O'Dell, V; O'Neil, D C; Obrant, G; Oguri, V; Oliveira, N; Oshima, N; Otec, R; Otero y Garzón, G J; Owen, M; Padley, P; Parashar, N; Park, S-J; Park, S K; Parsons, J; Partridge, R; Parua, N; Patwa, A; Pawloski, G; Perea, P M; Perez, E; Peters, K; Pétroff, P; Petteni, M; Piegaia, R; Pleier, M-A; Podesta-Lerma, P L M; Podstavkov, V M; Pogorelov, Y; Pol, M-E; Pompos, A; Pope, B G; Popov, A V; Prado da Silva, W L; Prosper, H B; Protopopescu, S; Qian, J; Quadt, A; Quinn, B; Rani, K J; Ranjan, K; Rapidis, P A; Ratoff, P N; Renkel, P; Reucroft, S; Rijssenbeek, M; Ripp-Baudot, I; Rizatdinova, F; Robinson, S; Rodrigues, R F; Royon, C; Rubinov, P; Ruchti, R; Rud, V I; Sajot, G; Sánchez-Hernández, A; Sanders, M P; Santoro, A; Savage, G; Sawyer, L; Scanlon, T; Schaile, D; Schamberger, R D; Scheglov, Y; Schellman, H; Schieferdecker, P; Schmitt, C; Schwanenberger, C; Schwartzman, A; Schwienhorst, R; Sengupta, S; Severini, H; Shabalina, E; Shamim, M; Shary, V; Shchukin, A A; Shephard, W D; Shivpuri, R K; Shpakov, D; Siccardi, V; Sidwell, R A; Simak, V; Sirotenko, V; Skubic, P; Slattery, P; Smith, R P; Snow, G R; Snow, J; Snyder, S; Söldner-Rembold, S; Song, X; Sonnenschein, L; Sopczak, A; Sosebee, M; Soustruznik, K; Souza, M; Spurlock, B; Stark, J; Steele, J; Stevenson, K; Stolin, V; Stone, A; Stoyanova, D A; Strandberg, J; Strang, M A; Strauss, M; Ströhmer, R; Strom, D; Strovink, M; Stutte, L; Sumowidagdo, S; Sznajder, A; Talby, M; Tamburello, P; Taylor, W; Telford, P; Temple, J; Tiller, B; Titov, M; Tokmenin, V V; Tomoto, M; Toole, T; Torchiani, I; Towers, S; Trefzger, T; Trincaz-Duvoid, S; Tsybychev, D; Tuchming, B; Tully, C; Turcot, A S; Tuts, P M; Unalan, R; Uvarov, L; Uvarov, S; Uzunyan, S; Vachon, B; van den Berg, P J; Kooten, R Van; van Leeuwen, W M; Varelas, N; Varnes, E W; Vartapetian, A; Vasilyev, I A; Vaupel, M; Verdier, P; Vertogradov, L S; Verzocchi, M; Villeneuve-Seguier, F; Vint, P; Vlimant, J-R; Von Toerne, E; Voutilainen, M; Vreeswijk, M; Wahl, H D; Wang, L; Warchol, J; Watts, G; Wayne, M; Weber, M; Weerts, H; Wermes, N; Wetstein, M; White, A; Wicke, D; Wilson, G W; Wimpenny, S J; Wobisch, M; Womersley, J; Wood, D R; Wyatt, T R; Xie, Y; Xuan, N; Yacoob, S; Yamada, R; Yan, M; Yasuda, T; Yatsunenko, Y A; Yip, K; Yoo, H D; Youn, S W; Yu, C; Yu, J; Yurkewicz, A; Zatserklyaniy, A; Zeitnitz, C; Zhang, D; Zhao, T; Zhao, Z; Zhou, B; Zhu, J; Zielinski, M; Zieminska, D; Zieminski, A; Zutshi, V; Zverev, E G

    2006-09-22

    A search for the production of neutral Higgs bosons Phi decaying into tau(+)tau(-) final states in pp[over ] collisions at a center-of-mass energy of 1.96 TeV is presented. The data, corresponding to an integrated luminosity of approximately 325 pb(-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 Phib(b[over ])-->bb[over ]b(b[over ]) and are interpreted in the minimal supersymmetric standard model. PMID:17025951

  13. 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.

  14. 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

  15. 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.; Prulhière, F.; Saadi, F.; Fearnley, T.; Hansen, J. D.; Hansen, J. R.; Hansen, P. H.; Møllerud, 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.; Rougé, 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.; Lütjens, G.; Lutz, G.; Männer, W.; Richter, R.; Rotscheidt, H.; Schröder, 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.; Lefrançois, 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.; Lançon, 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.; Johnson, R. P.; Litke, A. M.; Taylor, G.; Wear, J.; Ashman, J. G.; Babbage, W.; Booth, C. N.; Buttar, C.; Carney, R. E.; Cartwright, S.; Combley, F.; Hatfield, F.; Thompson, L. F.; Barberio, E.; Böhrer, A.; Brandt, S.; Cowan, G.; Grupen, C.; Lutters, G.; Rivera, F.; Schäfer, U.; Della Marina, R.; Giannini, G.; Gobbo, B.; Ragusa, F.; Bellantoni, L.; Chen, W.; Cinabro, D.; Conway, J. S.; Cowen, D. F.; Feng, Z.; Ferguson, D. P. S.; Gao, Y. S.; Grahl, J.; Harton, J. L.; Jared, R. C.; Leclaire, B. W.; Lishka, C.; Pan, Y. B.; Pater, J. R.; Saadi, Y.; Schmitt, M.; Sharma, V.; Shi, Z. H.; Walsh, A. M.; Weber, F. V.; Wu, Sau Lan; Wu, X.; Zheng, M.; Zobernig, G.

    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 τ→ ev bar v, τ→μ v bar v, τ→πν, τ→ρν and τ→ a 1ν, 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 τ and A e , where A l =2 g {/v l } g {/A l }/( g {/v l })2+( g {/A l })2] The results A τ=0.143±0.023 and A e =0.120±0.026 are consistent with the hypothesis of electron-tau universality. Assuming universality yields a measurement of the effective weak mixing angle sin2θ{/w eff}=0.2332±0.0022.

  16. Increased 4R-Tau Induces Pathological Changes in a Human-Tau Mouse Model.

    PubMed

    Schoch, Kathleen M; DeVos, Sarah L; Miller, Rebecca L; Chun, Seung J; Norrbom, Michaela; Wozniak, David F; Dawson, Hana N; Bennett, C Frank; Rigo, Frank; Miller, Timothy M

    2016-06-01

    Pathological evidence for selective four-repeat (4R) tau deposition in certain dementias and exon 10-positioned MAPT mutations together suggest a 4R-specific role in causing disease. However, direct assessments of 4R toxicity have not yet been accomplished in vivo. Increasing 4R-tau expression without change to total tau in human tau-expressing mice induced more severe seizures and nesting behavior abnormality, increased tau phosphorylation, and produced a shift toward oligomeric tau. Exon 10 skipping could also be accomplished in vivo, providing support for a 4R-tau targeted approach to target 4R-tau toxicity and, in cases of primary MAPT mutation, eliminate the disease-causing mutation. PMID:27210553

  17. Inhibition of tau aggregation by a rosamine derivative that blocks tau intermolecular disulfide cross-linking.

    PubMed

    Haque, Md Mamunul; Kim, Dohee; Yu, Young Hyun; Lim, Sungsu; Kim, Dong Jin; Chang, Young-Tae; Ha, Hyung-Ho; Kim, Yun Kyung

    2014-09-01

    Abnormal tau aggregates are presumed to be neurotoxic and are an important therapeutic target for multiple neurodegenerative disorders including Alzheimer's disease. Growing evidence has shown that tau intermolecular disulfide cross-linking is critical in generating tau oligomers that serve as a building block for higher-order aggregates. Here we report that a small molecule inhibitor prevents tau aggregation by blocking the generation of disulfide cross-linked tau oligomers. Among the compounds tested, a rosamine derivative bearing mild thiol reactivity selectively labeled tau and effectively inhibited oligomerization and fibrillization processes in vitro. Our data suggest that controlling tau oxidation status could be a new therapeutic strategy for prevention of abnormal tau aggregation. PMID:24919397

  18. Search for MSSM Higgs decaying to tau pairs in proton-antiproton collision at center of mass energy = 1.96 TeV at CDF

    NASA Astrophysics Data System (ADS)

    Jang, Dongwook

    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 int = 310 pb-1 are used. There is no evidence of MSSM Higgs existance, which results in the upper limits on sigma(pp¯ → φ) x BR(φ → tautau) in mA range between 115 and 250 GeV. These limits exclude some area in tan beta vs. mA parameter space.

  19. Evidence for a tau-neutrino mass

    SciTech Connect

    Samuel, M.A.; Mendel, R.R.

    1988-03-01

    In a recent experiment, the measured lifetime of the tau lepton indicates that the e - ..mu.. universality may not hold in the case of the third-generation leptons. It is shown here that the universality of weak interactions can be restored if the tau-neutrino has a non-zero mass. This results is m/sub v/tau/sub / = (160 +- 70) MeV.

  20. Distinct Therapeutic Mechanisms of Tau Antibodies

    PubMed Central

    Funk, Kristen E.; Mirbaha, Hilda; Jiang, Hong; Holtzman, David M.; Diamond, Marc I.

    2015-01-01

    Tauopathies are neurodegenerative diseases characterized by accumulation of Tau amyloids, and include Alzheimer disease and certain frontotemporal dementias. Trans-neuronal propagation of amyloid mediated by extracellular Tau may underlie disease progression. Consistent with this, active and passive vaccination studies in mouse models reduce pathology, although by unknown mechanisms. We previously reported that intracerebroventricular administration of three anti-Tau monoclonal antibodies (HJ8.5, HJ9.3, and HJ9.4) reduces pathology in a model overexpressing full-length mutant (P301S) human Tau. We now study effects of these three antibodies and a negative control antibody (HJ3.4) on Tau aggregate uptake into BV2 microglial-like cells and primary neurons. Antibody-independent Tau uptake into BV2 cells was blocked by heparin, consistent with a previously described role for heparan sulfate proteoglycans. Two therapeutic antibodies (HJ8.5 and HJ9.4) promoted uptake of full-length Tau fibrils into microglia via Fc receptors. Surprisingly, HJ9.3 promoted uptake of fibrils composed of the Tau repeat domain or Alzheimer disease-derived Tau aggregates, but failed to influence full-length recombinant Tau fibrils. Size fractionation of aggregates showed that antibodies preferentially promote uptake of larger oligomers (n ≥∼20-mer) versus smaller oligomers (n ∼10-mer) or monomer. No antibody inhibited uptake of full-length recombinant fibrils into primary neurons, but HJ9.3 blocked neuronal uptake of Tau repeat domain fibrils and Alzheimer disease-derived Tau. Antibodies thus have multiple potential mechanisms, including clearance via microglia and blockade of neuronal uptake. However these effects are epitope- and aggregate size-dependent. Establishing specific mechanisms of antibody activity in vitro may help in design and optimization of agents that are more effective in vivo. PMID:26126828

  1. 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.

  2. Formation and propagation of tau oligomeric seeds.

    PubMed

    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

  3. Top pair production in the dilepton decay channel with a tau lepton

    SciTech Connect

    Corbo, Matteo

    2012-09-19

    The top quark pair production and decay into leptons with at least one being a τ lepton is studied in the framework of the CDF experiment at the Tevatron proton antiproton collider at Fermilab (USA). The selection requires an electron or a muon produced either by the τ lepton decay or by a W decay. The analysis uses the complete Run II data set i.e. 9.0 fb-1, selected by one trigger based on a low transverse momentum electron or muon plus one isolated charged track. The top quark pair production cross section at 1.96 TeV is measured at 8.2 ± 1.7+1.2-1.1 ± 0.5 pb, and the top branching ratio into τ lepton is measured at 0.120 ± 0.027+0.022 -0.019 ± 0.007 with statistical, systematics and luminosity uncertainties. These are up to date the most accurate results in this top decay channel and are in good agreement with the results obtained using other decay channels of the top at the Tevatron. The branching ratio is also measured separating the single lepton from the two leptons events with a log likelihood method. This is the first time these two signatures are separately identified. With a fit to data along the log-likelihood variable an alternative measurement of the branching ratio is made: 0.098 ± 0.022(stat:) ± 0.014(syst:); it is in good agreement with the expectations of the Standard Model (with lepton universality) within the experimental uncertainties. The branching ratio is constrained to be less than 0.159 at 95% con dence level. This limit translates into a limit of a top branching ratio into a potential charged Higgs boson.

  4. Reactive microglia drive tau pathology and contribute to the spreading of pathological tau in the brain

    PubMed Central

    Maphis, Nicole; Xu, Guixiang; Kokiko-Cochran, Olga N.; Jiang, Shanya; Cardona, Astrid; Ransohoff, Richard M.; Lamb, Bruce T.

    2015-01-01

    Pathological aggregation of tau is a hallmark of Alzheimer’s disease and related tauopathies. We have previously shown that the deficiency of the microglial fractalkine receptor (CX3CR1) led to the acceleration of tau pathology and memory impairment in an hTau mouse model of tauopathy. Here, we show that microglia drive tau pathology in a cell-autonomous manner. First, tau hyperphosphorylation and aggregation occur as early as 2 months of age in hTauCx3cr1−/− mice. Second, CD45+ microglial activation correlates with the spatial memory deficit and spread of tau pathology in the anatomically connected regions of the hippocampus. Third, adoptive transfer of purified microglia derived from hTauCx3cr1−/− mice induces tau hyperphosphorylation within the brains of non-transgenic recipient mice. Finally, inclusion of interleukin 1 receptor antagonist (Kineret®) in the adoptive transfer inoculum significantly reduces microglia-induced tau pathology. Together, our results suggest that reactive microglia are sufficient to drive tau pathology and correlate with the spread of pathological tau in the brain. PMID:25833819

  5. 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

  6. Productions of K_1(1400) and K_1(1270) in tau Decays

    NASA Astrophysics Data System (ADS)

    Li, Bing An

    1996-05-01

    In an effective chiral theory of mesons the K_1(1400) meson field is expressed by an axial-vector current of quarks. Therefore, this meson can be produced in τ decay(τarrow K_1(1400) ν) at the three level. In order to test the expression of K_1(1400), the mass of this meson is calculated (m^2_K_1(1400)=g^2_a\\over g^2_ρ(m^2_ρ+ m^2_K^*(892))), where ga and g_ρ are determined explicitly. The partial widths of three decay channels(K1 arrow K^*π, Kρ, and Kω) are computed. Theoretical results are in good agreement with data. In the chiral limit, the coupling constant between K_1(1400) and W-boson is ga and the theoretical prediction of B( τarrow K_1(1400)ν) is 0.37% and the experiment value is 0.76^+0.40_-0.33%. There is no new parameter in all these calculations and the parameters are determined by other fits. In this effective chiral theory K_1(1270) meson field is expressed by a different quark operator and this field is not coupled to W-boson directly. Therefore, τarrow K_1(1270)ν is forbidden at the tree level. However, at one loop level this decay is allowed. Large NC expansion is a natural result of this effective theory. At the three level the amplitude of τarrow K_1(1400)ν is at O(N_C) and the amplitude of τarrow K_1(1270)ν is at O. Comparing to τarrow K_1(1400)ν the amplitude of τarrow K_1(1270)ν is suppressed by O(1/N_c).

  7. 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.

  8. 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.

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

    SciTech Connect

    Schenk, Stefan

    2008-07-07

    This work presents simultaneous branching fraction measurements of the decay modes τ- → K-0ντ with n = 0,1,2,3 and τ- → π-0ντ with n = 3,4. The analysis is based on a data sample of 427 x 106 τ+τ- pairs recorded with the BABAR detector, which corresponds to an integrated luminosity of 464.4 fb-1. The measured values are β(τ- → K-ντ ) = (6.57 ± 0.03 ± 0.11) x 10-3, β(τ- → K-π0ντ ) = (4.61 ± 0.03 ± 0.11) x 10-3, β(τ- {yields} K- π0π0ντ) = (5.05 ± 0.17 ± 0.44) x 10-4, β(τ- {yields} K-π0π0π0ντ ) = (1.31 ± 0.43 ± 0.40) x 10-4, β(τ0 → π0π0π0π0ντ) = (1.263 ± 0.008 ± 0.078) x 10-2 and β(τ0 → π0π0π0π0π0ντ) = (9.6 ± 0.5 ± 1.2) x 10-4, 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 β(τ0 → π-π0π0π0π0vτ) 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 |Vus| from hadronic τ decays yields |Vus| = 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.

  10. 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 \

  11. Intrinsic Tau Acetylation Is Coupled to Auto-Proteolytic Tau Fragmentation

    PubMed Central

    Cohen, Todd J.; Constance, Brian H.; Hwang, Andrew W.; James, Michael; Yuan, Chao-Xing

    2016-01-01

    Tau proteins are abnormally aggregated in a range of neurodegenerative tauopathies including Alzheimer’s disease (AD). Recently, tau has emerged as an extensively post-translationally modified protein, among which lysine acetylation is critical for normal tau function and its pathological aggregation. Here, we demonstrate that tau isoforms have different propensities to undergo lysine acetylation, with auto-acetylation occurring more prominently within the lysine-rich microtubule-binding repeats. Unexpectedly, we identified a unique intrinsic property of tau in which auto-acetylation induces proteolytic tau cleavage, thereby generating distinct N- and C-terminal tau fragments. Supporting a catalytic reaction-based mechanism, mapping and mutagenesis studies showed that tau cysteines, which are required for acetyl group transfer, are also essential for auto-proteolytic tau processing. Further mass spectrometry analysis identified the C-terminal 2nd and 4th microtubule binding repeats as potential sites of auto-cleavage. The identification of acetylation-mediated auto-proteolysis provides a new biochemical mechanism for tau self-regulation and warrants further investigation into whether auto-catalytic functions of tau are implicated in AD and other tauopathies. PMID:27383765

  12. 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.

  13. New Features about Tau Function and Dysfunction

    PubMed Central

    Medina, Miguel; Hernández, Félix; Avila, Jesús

    2016-01-01

    Tau is a brain microtubule-associated protein that directly binds to a microtubule and dynamically regulates its structure and function. Under pathological conditions, tau self-assembles into filamentous structures that end up forming neurofibrillary tangles. Prominent tau neurofibrillary pathology is a common feature in a number of neurodegenerative disorders, collectively referred to as tauopathies, the most common of which is Alzheimer’s disease (AD). Beyond its classical role as a microtubule-associated protein, recent advances in our understanding of tau cellular functions have revealed novel insights into their important role during pathogenesis and provided potential novel therapeutic targets. Regulation of tau behavior and function under physiological and pathological conditions is mainly achieved through post-translational modifications, including phosphorylation, glycosylation, acetylation, and truncation, among others, indicating the complexity and variability of factors influencing regulation of tau toxicity, all of which have significant implications for the development of novel therapeutic approaches in various neurodegenerative disorders. A more comprehensive understanding of the molecular mechanisms regulating tau function and dysfunction will provide us with a better outline of tau cellular networking and, hopefully, offer new clues for designing more efficient approaches to tackle tauopathies in the near future. PMID:27104579

  14. CHIP-ping away at tau.

    PubMed

    Goryunov, Dmitry; Liem, Ronald K H

    2007-03-01

    Protein accumulation is a hallmark of many neurodegenerative disorders. In Alzheimer's disease (AD), a hyperphosphorylated form of the protein tau (p-tau) forms intracellular inclusions known as neurofibrillary tangles. Deposits of p-tau have also been found in the brains of patients with Down's syndrome, supranuclear palsy, and prion disease. Mutations in tau have been causally associated with at least one inherited neurologic disorder, frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17), implying that tau abnormalities by themselves can be a primary cause of degenerative diseases of the CNS. Removal of these p-tau species may occur by both chaperone-mediated refolding and degradation. In this issue of the JCI, Dickey and colleagues show that a cochaperone protein, carboxyl terminus of Hsp70-interacting protein (CHIP), in a complex with Hsp90 plays an important role in the removal of p-tau (see the related article beginning on page 648). Pharmacologic manipulation of Hsp90 may be used to alleviate p-tau accumulation in disease. PMID:17332887

  15. New Features about Tau Function and Dysfunction.

    PubMed

    Medina, Miguel; Hernández, Félix; Avila, Jesús

    2016-01-01

    Tau is a brain microtubule-associated protein that directly binds to a microtubule and dynamically regulates its structure and function. Under pathological conditions, tau self-assembles into filamentous structures that end up forming neurofibrillary tangles. Prominent tau neurofibrillary pathology is a common feature in a number of neurodegenerative disorders, collectively referred to as tauopathies, the most common of which is Alzheimer's disease (AD). Beyond its classical role as a microtubule-associated protein, recent advances in our understanding of tau cellular functions have revealed novel insights into their important role during pathogenesis and provided potential novel therapeutic targets. Regulation of tau behavior and function under physiological and pathological conditions is mainly achieved through post-translational modifications, including phosphorylation, glycosylation, acetylation, and truncation, among others, indicating the complexity and variability of factors influencing regulation of tau toxicity, all of which have significant implications for the development of novel therapeutic approaches in various neurodegenerative disorders. A more comprehensive understanding of the molecular mechanisms regulating tau function and dysfunction will provide us with a better outline of tau cellular networking and, hopefully, offer new clues for designing more efficient approaches to tackle tauopathies in the near future. PMID:27104579

  16. Large tau and tau neutrino electric dipole moments in models with vectorlike multiplets

    SciTech Connect

    Ibrahim, Tarek; Nath, Pran

    2010-02-01

    It is shown that the electric dipole moment of the {tau} lepton several orders of magnitude larger than predicted by the standard model can be generated from mixings in models with vectorlike mutiplets. The electric dipole moment (EDM) of the {tau} lepton arises from loops involving the exchange of the W, the charginos, the neutralinos, the sleptons, the mirror leptons, and the mirror sleptons. The EDM of the Dirac {tau} neutrino is also computed from loops involving the exchange of the W, the charginos, the mirror leptons, and the mirror sleptons. A numerical analysis is presented, and it is shown that the EDMs of the {tau} lepton and the {tau} neutrino which lie just a couple of orders of magnitude below the sensitivity of the current experiment can be achieved. Thus the predictions of the model are testable in an improved experiment on the EDM of the {tau} and the {tau} neutrino.

  17. Tau pathology-mediated presynaptic dysfunction.

    PubMed

    Moreno, H; Morfini, G; Buitrago, L; Ujlaki, G; Choi, S; Yu, E; Moreira, J E; Avila, J; Brady, S T; Pant, H; Sugimori, M; Llinás, R R

    2016-06-14

    Brain tauopathies are characterized by abnormal processing of tau protein. While somatodendritic tau mislocalization has attracted considerable attention in tauopathies, the role of tau pathology in axonal transport, connectivity and related dysfunctions remains obscure. We have previously shown using the squid giant synapse that presynaptic microinjection of recombinant human tau protein (htau42) results in failure of synaptic transmission. Here, we evaluated molecular mechanisms mediating this effect. Thus, the initial event, observed after htau42 presynaptic injection, was an increase in transmitter release. This event was mediated by calcium release from intracellular stores and was followed by a reduction in evoked transmitter release. The effect of htau42 on synaptic transmission was recapitulated by a peptide comprising the phosphatase-activating domain of tau, suggesting activation of phosphotransferases. Accordingly, findings indicated that htau42-mediated toxicity involves the activities of both GSK3 and Cdk5 kinases. PMID:27012611

  18. A Search for the Standard Model Higgs Boson Produced in Association with a Vector Boson and Decaying to a Hadronically-Decaying Tau Pair at ATLAS

    NASA Astrophysics Data System (ADS)

    Ideal, Emma Anne

    On July 4, 2012, the discovery of the Higgs boson was simultaneously announced by the ATLAS and CMS collaborations. Since then, evidence for H →ττ has been claimed. As of now, there have been no Higgs discoveries in any of its associated production modes. For this thesis, a search for the Higgs boson produced in association with a vector boson V = W+/-, Z and decaying to a tau lepton pair was conducted using 2012 ATLAS data. The data corresponds to 20.3 f3-1 of 8 TeV center-of-mass energy proton-proton collisions delivered by the LHC. This analysis focuses on the search in the WH and ZH categories in which the Higgs boson decays to a pair of hadronically decaying taus. In order to better identify this signature in the midst of overwhelming hadronic activity, the vector bosons are required to decay leptonically. A data-driven multi-lepton fake factor method is used as the primary background estimation technique, modeling all reducible backgrounds where jets are misidentified as hadronic taus; Monte Carlo simulation is used to model the irreducible diboson backgrounds. There are insufficient statistics in the 2012 dataset to discover the Standard Model (SM) Higgs boson in these categories, so 95% confidence-level upper limits on the SM Higgs associated production cross section times the H →ττ branching ratio are calculated. For a Higgs boson mass mH = 125 GeV, an upper limit of 5.3 times the SM Higgs cross section is expected.

  19. Tau monoclonal antibody generation based on humanized yeast models: impact on Tau oligomerization and diagnostics.

    PubMed

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

    2015-02-13

    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 Tyr(18). 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

  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. Characteristics of Tau and Its Ligands in PET Imaging

    PubMed Central

    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 β-sheet binding properties, and the status of tau imaging in clinical studies. PMID:26751494

  2. AMP-activated protein kinase modulates tau phosphorylation and tau pathology in vivo

    PubMed Central

    Domise, Manon; Didier, Sébastien; Marinangeli, Claudia; Zhao, Haitian; Chandakkar, Pallavi; Buée, Luc; Viollet, Benoit; Davies, Peter; Marambaud, Philippe; Vingtdeux, Valérie

    2016-01-01

    Neurofibrillary tangles (NFTs) are the pathological hallmark of neurodegenerative diseases commonly known as tauopathies. NFTs result from the intracellular aggregation of abnormally and hyperphosphorylated tau proteins. Tau functions, which include the regulation of microtubules dynamics, are dependent on its phosphorylation status. As a consequence, any changes in tau phosphorylation can have major impacts on synaptic plasticity and memory. Recently, it has been demonstrated that AMP-activated protein kinase (AMPK) was deregulated in the brain of Alzheimer’s disease (AD) patients where it co-localized with phosphorylated tau in pre-tangle and tangle-bearing neurons. Besides, it was found that AMPK was a tau kinase in vitro. Here, we find that endogenous AMPK activation in mouse primary neurons induced an increase of tau phosphorylation at multiple sites, whereas AMPK inhibition led to a rapid decrease of tau phosphorylation. We further show that AMPK mice deficient for one of the catalytic alpha subunits displayed reduced endogenous tau phosphorylation. Finally, we found that AMPK deficiency reduced tau pathology in the PS19 mouse model of tauopathy. These results show that AMPK regulates tau phosphorylation in mouse primary neurons as well as in vivo, and thus suggest that AMPK could be a key player in the development of AD pathology. PMID:27230293

  3. AMP-activated protein kinase modulates tau phosphorylation and tau pathology in vivo.

    PubMed

    Domise, Manon; Didier, Sébastien; Marinangeli, Claudia; Zhao, Haitian; Chandakkar, Pallavi; Buée, Luc; Viollet, Benoit; Davies, Peter; Marambaud, Philippe; Vingtdeux, Valérie

    2016-01-01

    Neurofibrillary tangles (NFTs) are the pathological hallmark of neurodegenerative diseases commonly known as tauopathies. NFTs result from the intracellular aggregation of abnormally and hyperphosphorylated tau proteins. Tau functions, which include the regulation of microtubules dynamics, are dependent on its phosphorylation status. As a consequence, any changes in tau phosphorylation can have major impacts on synaptic plasticity and memory. Recently, it has been demonstrated that AMP-activated protein kinase (AMPK) was deregulated in the brain of Alzheimer's disease (AD) patients where it co-localized with phosphorylated tau in pre-tangle and tangle-bearing neurons. Besides, it was found that AMPK was a tau kinase in vitro. Here, we find that endogenous AMPK activation in mouse primary neurons induced an increase of tau phosphorylation at multiple sites, whereas AMPK inhibition led to a rapid decrease of tau phosphorylation. We further show that AMPK mice deficient for one of the catalytic alpha subunits displayed reduced endogenous tau phosphorylation. Finally, we found that AMPK deficiency reduced tau pathology in the PS19 mouse model of tauopathy. These results show that AMPK regulates tau phosphorylation in mouse primary neurons as well as in vivo, and thus suggest that AMPK could be a key player in the development of AD pathology. PMID:27230293

  4. Phosphorylated tau and the neurodegenerative foldopathies.

    PubMed

    Kosik, Kenneth S; Shimura, Hideki

    2005-01-01

    Many studies have implicated phosphorylated tau in the Alzheimer disease process. However, the cellular fate of phosphorylated tau has only recently been described. Recent work has shown that tau phosphorylation at substrate sites for the kinases Cdk5 and GSK3-beta can trigger the binding of tau to the chaperones Hsc70 and Hsp27. The binding of phosphorylated tau to Hsc70 implied that the complex may be a substrate for the E3 ligase CHIP and this possibility was experimentally verified. The presence of this system in cells suggests that phosphorylated tau may hold toxic dangers for cell viability, and the response of the cell is to harness a variety of protective mechanisms. These include binding to chaperones, which may prevent more toxic conformations of the protein, ubiquitination which will direct the protein to the proteasome, segregation of tau aggregates from the cellular machinery, and recruitment of Hsp27 which will confer anti-apoptotic properties to the cell. PMID:15615647

  5. Recent Results on Charm and Tau Physics from BaBar And Belle

    SciTech Connect

    Salvatore, Fabrizio F.; /Royal Holloway, U. of London

    2007-10-15

    Recent results on charm and tau physics obtained at the BABAR and Belle experiments are presented in this article. The charm section will be focused on the most recent results on D{sup 0}{bar D}{sup 0} mixing at Belle and on the measurement of the pseudoscalar decay constant f{sub Ds} using charm tagged e+e- events at BABAR. In the tau section the recent results on Lepton Flavor Violation from tau decays will be discussed, as well as the recent result on the rare decay {tau}{sup -} {yields} 3{pi}{sup -}2{pi}{sup +}2{pi}{sup 0}{nu}{sub {tau}} at BABAR and the measurement of the {tau} lepton mass at Belle.

  6. Lepton flavor violating Higgs bosons and {tau}{yields}{mu}{gamma}

    SciTech Connect

    Davidson, Sacha; Grenier, Gerald

    2010-05-01

    We update phenomenological constraints on a two Higgs doublet model with lepton flavor nonconserving Yukawa couplings. We review that tan{beta} is ambiguous in such 'type III' models, and define it from the {tau} Yukawa coupling. The neutral scalars {phi} could be searched for at hadron colliders in {phi}{yields}{tau}{mu} and are constrained by the rare decay {tau}{yields}{mu}{gamma}. The Feynman diagrams for the collider process, with Higgs production via gluon fusion, are similar to the two-loop ''Barr-Zee'' diagrams, which contribute to {tau}{yields}{mu}{gamma}. Some ''tuning'' is required to obtain a collider cross section of order the standard model expectation for {sigma}(gg{yields}h{sub SM{yields}{tau}}{sup +{tau}-}), while agreeing with the current bound from {tau}{yields}{mu}{gamma}.

  7. Tau and muon lepton flavor violations in the littlest Higgs model with T parity

    SciTech Connect

    Goto, Toru; Okada, Yasuhiro; Yamamoto, Yasuhiro

    2011-03-01

    Lepton flavor violation in {tau} and {mu} processes is studied in the littlest Higgs model with T parity. We consider various asymmetries defined in polarized {tau} and {mu} decays. Correlations among branching ratios and asymmetries are shown in the following lepton flavor violation processes: {mu}{sup +}{yields}e{sup +}{gamma}, {mu}{sup +}{yields}e{sup +}e{sup +}e{sup -}, {mu}{sup -}A{yields}e{sup -}A (A=Al, Ti, Au, and Pb), {tau}{sup +}{yields}{mu}{sup +}{gamma}, {tau}{sup +}{yields}{mu}{sup +}{mu}{sup +}{mu}{sup -}, {tau}{sup +}{yields}{mu}{sup +}e{sup +}e{sup -}, {tau}{sup +}{yields}{mu}{sup +}P (P={pi}{sup 0}, {eta} and {eta}{sup '}), {tau}{sup +}{yields}{mu}{sup +}V (V={rho}{sup 0}, {omega} and {phi}), {tau}{sup +}{yields}e{sup +}{gamma}, {tau}{sup +}{yields}e{sup +}e{sup +}e{sup -}, {tau}{sup +}{yields}e{sup +}{mu}{sup +}{mu}{sup -}, {tau}{sup +}{yields}e{sup +}P, {tau}{sup +}{yields}e{sup +}V, {tau}{sup +}{yields}{mu}{sup +}{mu}{sup +}e{sup -} and {tau}{sup +}{yields}e{sup +}e{sup +}{mu}{sup -}. It is shown that large parity asymmetries and time-reversal asymmetries are allowed in {mu}{sup +}{yields}e{sup +}e{sup +}e{sup -}. For {tau} lepton flavor violation processes, sizable asymmetries are possible reflecting characteristic chirality structure of lepton flavor violating interactions in this model.

  8. 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.

  9. 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

  10. 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

  11. 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

  12. 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 Δ 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.

  13. Park2-null/tau transgenic mice reveal a functional relationship between parkin and tau.

    PubMed

    Guerrero, Rosa; Navarro, Paloma; Gallego, Eva; Avila, Jesus; de Yebenes, Justo G; Sanchez, Marina P

    2008-03-01

    Mutations, haplotypes, and polymorphisms of tau and Park-2 genes constitute risk factors for developing tauopathies. In order to analyze the possible relationship between parkin and tau we generated a double-mutant mouse deficient for Park-2 expression and overexpressing a mutant tau protein (hTauVLW). Mice develop normally, although the median survival rate is considerably reduced with respect to wild type (45%). Aggregates of phosphorylated tau in neurons and reactive gliosis are quite abundant in cortex and hippocampus of these mice. Moreover, while in young transgenic mice the hTauVLW immunostained transgene product is observed in both cell bodies and dendrites, the hTauVLW mutant protein is only detected in the neuronal cell bodies when Park-2 gene is additionally deleted. Moreover, DNA fragmentation was detected by the TUNEL method, and cerebral atrophy is also present in these regions. The levels of phosphorylated tau and Hsp70 are increased in the double-mutant mice, while CHIP expression in hippocampus is lower when the Park-2 gene is deleted. Thus, the combination of Park-2 gene deletion with hTauVLW transgene overexpression in mice produces serious neuropathological effects, which reflect the existence of some relationship between both proteins. PMID:18376058

  14. 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

  15. 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

  16. The winds from HL Tau

    PubMed Central

    Klaassen, P. D.; Mottram, J. C.; Maud, L. T.; Juhasz, A.

    2016-01-01

    Outflowing motions, whether a wind launched from the disc, a jet launched from the protostar, or the entrained molecular outflow, appear to be a ubiquitous feature of star formation. These outwards motions have a number of root causes, and how they manifest is intricately linked to their environment as well as the process of star formation itself. Using the Atacama Large Millimeter/submillimeter Array (ALMA) Science Verification data of HL Tau, we investigate the high-velocity molecular gas being removed from the system as a result of the star formation process. We aim to place these motions in context with the optically detected jet, and the disc. With these high-resolution (∼1 arcsec) ALMA observations of CO (J=1−0), we quantify the outwards motions of the molecular gas. We find evidence for a bipolar outwards flow, with an opening angle, as measured in the redshifted lobe, starting off at 90°, and narrowing to 60° further from the disc, likely because of magnetic collimation. Its outwards velocity, corrected for inclination angle is of the order of 2.4 km s−1. PMID:27559304

  17. The winds from HL Tau

    NASA Astrophysics Data System (ADS)

    Klaassen, P. D.; Mottram, J. C.; Maud, L. T.; Juhasz, A.

    2016-07-01

    Outflowing motions, whether a wind launched from the disc, a jet launched from the protostar, or the entrained molecular outflow, appear to be a ubiquitous feature of star formation. These outwards motions have a number of root causes, and how they manifest is intricately linked to their environment as well as the process of star formation itself. Using the Atacama Large Millimeter/submillimeter Array (ALMA) Science Verification data of HL Tau, we investigate the high-velocity molecular gas being removed from the system as a result of the star formation process. We aim to place these motions in context with the optically detected jet, and the disc. With these high-resolution (˜1 arcsec) ALMA observations of CO (J=1-0), we quantify the outwards motions of the molecular gas. We find evidence for a bipolar outwards flow, with an opening angle, as measured in the redshifted lobe, starting off at 90°, and narrowing to 60° further from the disc, likely because of magnetic collimation. Its outwards velocity, corrected for inclination angle is of the order of 2.4 km s-1.

  18. The winds from HL Tau

    NASA Astrophysics Data System (ADS)

    Klaassen, P. D.; Mottram, J. C.; Maud, L. T.; Juhasz, A.

    2016-04-01

    Outflowing motions, whether a wind launched from the disk, a jet launched from the protostar, or the entrained molecular outflow, appear to be an ubiquitous feature of star formation. These outwards motions have a number of root causes, and how they manifest is intricately linked to their environment as well as the process of star formation itself. Using the ALMA Science Verification data of HL Tau, we investigate the high velocity molecular gas being removed from the system as a result of the star formation process. We aim to place these motions in context with the optically detected jet, and the disk. With these high resolution (˜1″) ALMA observations of CO (J=1-0), we quantify the outwards motions of the molecular gas. We find evidence for a bipolar outwards flow, with an opening angle, as measured in the red-shifted lobe, starting off at 90°, and narrowing to 60° further from the disk, likely because of magnetic collimation. Its outwards velocity, corrected for inclination angle is of order 2.4 km s-1.

  19. 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}.

  20. 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.

  1. Tau protein binds to pericentromeric DNA: a putative role for nuclear tau in nucleolar organization.

    PubMed

    Sjöberg, Marcela K; Shestakova, Elena; Mansuroglu, Zeyni; Maccioni, Ricardo B; Bonnefoy, Eliette

    2006-05-15

    The microtubule-associated tau protein participates in the organization and integrity of the neuronal cytoskeleton. A nuclear form of tau has been described in neuronal and non-neuronal cells, which displays a nucleolar localization during interphase but is associated with nucleolar-organizing regions in mitotic cells. In the present study, based on immunofluorescence, immuno-FISH and confocal microscopy, we show that nuclear tau is mainly present at the internal periphery of nucleoli, partially colocalizing with the nucleolar protein nucleolin and human AT-rich alpha-satellite DNA sequences organized as constitutive heterochromatin. By using gel retardation, we demonstrate that tau not only colocalizes with, but also specifically binds to, AT-rich satellite DNA sequences apparently through the recognition of AT-rich DNA stretches. Here we propose a functional role for nuclear tau in relation to the nucleolar organization and/or heterochromatinization of a portion of RNA genes. Since nuclear tau has also been found in neurons from patients with Alzheimer's disease (AD), aberrant nuclear tau could affect the nucleolar organization during the course of AD. We discuss nucleolar tau associated with AT-rich alpha-satellite DNA sequences as a potential molecular link between trisomy 21 and AD. PMID:16638814

  2. 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.

  3. 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.

  4. 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

  5. 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 0.06–0.30 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

  6. 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.

    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.

  7. 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.

  8. Search for charged Higgs Bosons decaying via {H(+) -> tau_{lep.} + nu} in {tbar{t}} events at {sqrt{s}=7textrm{ TeV}} in ATLAS

    NASA Astrophysics Data System (ADS)

    Breaden Madden, William Dmitri Morgan

    This thesis for the degree of Master of Science by Research presents the theory, methodology and results of a search for charged Higgs bosons decaying via {H. + -> tau_{lep.} + nu} using single lepton and two lepton channels in {t} quark pair ({tbar{t}}) events with a leptonically decaying {tau} in the final state based on {1.03textrm{ fb}. {-1}} of proton-proton collision data at centre of mass energy {sqrt{s}=7textrm{ TeV}} from ATLAS, an experiment of the LHC, with special attention given to the statistical analysis and calculation involved in the limit setting process. For the single lepton channel, the expected number of Standard Model-like {tbar{t} -> bbar{b}W. {+}W. {-}} background events lies between 0.99 and 1.03 times the Standard Model prediction, with uncertainties in the range {2%} - {3%}. For the two lepton channel, the expected number of Standard Model-like background events lies between 0.99 and 1.03 times the Standard Model prediction, with uncertainties in the range {5%} - {25%}. Assuming the branching fraction {mathcal{B}≤ft(H. {+} -> taumuright)=1}, the upper limits on the branching fraction {mathcal{B}≤ft(t -> bH. {+}right)} at the 95% confidence level are between {5.2%} and {14.1%} for charged Higgs boson masses in the range {90textrm{ GeV}≤ m_{H. {+}}≤ 160textrm{ GeV}}. In the context of the {m. {textrm{max.}}_{h}} scenario of the MSSM, values of {tanbeta} greater than {30}-{56} are excluded in the mass range {90textrm{ GeV}≤ m_{H. {+}}≤ 140textrm{ GeV}}. The compatibility with background of the combination of the single lepton and two lepton channels ranges between {26%} and {50%}, as measured by {p_{0}} values. Hence, no indication of a {H. {+}}-like excess is found.

  9. Inhibition of Both Hsp70 Activity and Tau Aggregation in Vitro Best Predicts Tau Lowering Activity of Small Molecules.

    PubMed

    Martin, Mackenzie D; Baker, Jeremy D; Suntharalingam, Amirthaa; Nordhues, Bryce A; Shelton, Lindsey B; Zheng, Dali; Sabbagh, Jonathan J; Haystead, Timothy A J; Gestwicki, Jason E; Dickey, Chad A

    2016-07-15

    Three scaffolds with inhibitory activity against the heat shock protein 70 (Hsp70) family of chaperones have been found to enhance the degradation of the microtubule associated protein tau in cells, neurons, and brain tissue. This is important because tau accumulation is linked to neurodegenerative diseases including Alzheimer's disease (AD) and chronic traumatic encephalopathy (CTE). Here, we expanded upon this study to investigate the anti-tau efficacy of additional scaffolds with Hsp70 inhibitory activity. Five of the nine scaffolds tested lowered tau levels, with the rhodacyanine and phenothiazine scaffolds exhibiting the highest potency as previously described. Because phenothiazines also inhibit tau aggregation in vitro, we suspected that this activity might be a more accurate predictor of tau lowering. Interestingly, the rhodacyanines did inhibit in vitro tau aggregation to a similar degree as phenothiazines, correlating well with tau-lowering efficacy in cells and ex vivo slices. Moreover, other Hsp70 inhibitor scaffolds with weaker tau-lowering activity in cells inhibited tau aggregation in vitro, albeit at lower potencies. When we tested six well-characterized tau aggregation inhibitors, we determined that this mechanism of action was not a better predictor of tau-lowering than Hsp70 inhibition. Instead, we found that compounds possessing both activities were the most effective at promoting tau clearance. Moreover, cytotoxicity and PAINS activity are critical factors that can lead to false-positive lead identification. Strategies designed around these principles will likely yield more efficacious tau-lowering compounds. PMID:27177119

  10. 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.

  11. 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

  12. 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

  13. Microtubule-associated protein tau in bovine retinal photoreceptor rod outer segments: comparison with brain tau.

    PubMed

    Yamazaki, Akio; Nishizawa, Yuji; Matsuura, Isao; Hayashi, Fumio; Usukura, Jiro; Bondarenko, Vladimir A

    2013-10-01

    Recent studies have suggested a possible involvement of abnormal tau in some retinal degenerative diseases. The common view in these studies is that these retinal diseases share the mechanism of tau-mediated degenerative diseases in brain and that information about these brain diseases may be directly applied to explain these retinal diseases. Here we collectively examine this view by revealing three basic characteristics of tau in the rod outer segment (ROS) of bovine retinal photoreceptors, i.e., its isoforms, its phosphorylation mode and its interaction with microtubules, and by comparing them with those of brain tau. We find that ROS contains at least four isoforms: three are identical to those in brain and one is unique in ROS. All ROS isoforms, like brain isoforms, are modified with multiple phosphate molecules; however, ROS isoforms show their own specific phosphorylation pattern, and these phosphorylation patterns appear not to be identical to those of brain tau. Interestingly, some ROS isoforms, under the normal conditions, are phosphorylated at the sites identical to those in Alzheimer's patient isoforms. Surprisingly, a large portion of ROS isoforms tightly associates with a membranous component(s) other than microtubules, and this association is independent of their phosphorylation states. These observations strongly suggest that tau plays various roles in ROS and that some of these functions may not be comparable to those of brain tau. We believe that knowledge about tau in the entire retinal network and/or its individual cells are also essential for elucidation of tau-mediated retinal diseases, if any. PMID:23712071

  14. Tau physics at p[bar p] colliders

    SciTech Connect

    Konigsberg, J. . High Energy Physics Lab.)

    1993-01-01

    Tau detection techniques in hadron colliders are discussed together with the measurements and searches performed so far. We also underline the importance tau physics has in present and future collider experiments.

  15. Tau physics at p{bar p} colliders

    SciTech Connect

    Konigsberg, J.

    1993-01-01

    Tau detection techniques in hadron colliders are discussed together with the measurements and searches performed so far. We also underline the importance tau physics has in present and future collider experiments.

  16. Tau phosphorylation at Alzheimer's disease-related Ser356 contributes to tau stabilization when PAR-1/MARK activity is elevated.

    PubMed

    Ando, Kanae; Oka, Mikiko; Ohtake, Yosuke; Hayashishita, Motoki; Shimizu, Sawako; Hisanaga, Shin-Ichi; Iijima, Koichi M

    2016-09-16

    Abnormal phosphorylation of the microtubule-associated protein tau is observed in many neurodegenerative diseases, including Alzheimer's disease (AD). AD-related phosphorylation of two tau residues, Ser262 and Ser356, by PAR-1/MARK stabilizes tau in the initial phase of mismetabolism, leading to subsequent phosphorylation events, accumulation, and toxicity. However, the relative contribution of phosphorylation at each of these sites to tau stabilization has not yet been elucidated. In a Drosophila model of human tau toxicity, we found that tau was phosphorylated at Ser262, but not at Ser356, and that blocking Ser262 phosphorylation decreased total tau levels. By contrast, when PAR-1 was co-overexpressed with tau, tau was hyperphosphorylated at both Ser262 and Ser356. Under these conditions, the protein levels of tau were significantly elevated, and prevention of tau phosphorylation at both residues was necessary to completely suppress this elevation. These results suggest that tau phosphorylation at Ser262 plays the predominant role in tau stabilization when PAR-1/MARK activity is normal, whereas Ser356 phosphorylation begins to contribute to this process when PAR-1/MARK activity is abnormally elevated, as in diseased brains. PMID:27520376

  17. 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.

  18. 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.

  19. Microglial tau undergoes phosphorylation-independent modification after ischemia.

    PubMed

    Uchihara, Toshiki; Nakamura, Ayako; Arai, Tetsuaki; Ikeda, Kenji; Tsuchiya, Kuniaki

    2004-01-15

    Tau2 is a phosphorylation-independent antibody that immunolabels neurofibrillary tangles (NFTs) of Alzheimer type and microglia around ischemic foci on formalin-fixed, paraffin-embedded sections. We found that copresence of polyethyleneglycol-p-isooctylphenyl ether (Triton X-100; TX) with tau2 abolished its immunoreactivity (IR) in these microglia but not its IR on NFTs. Tau2-immunoreactive bands, exclusively retrieved in Tris-soluble fraction of brain homogenates from ischemic foci, normal human and bovine brains, were of similar electrophoretic mobility, indicating that tau2 IR in these microglia is unrelated to hyperphosphorylation of tau. These tau2-immunoreactive bands except those from bovine brain were abolished in the copresence of TX. This was not due to washing out of tau, because similar immunoreactive bands were detectable with another antitau antibody even under a higher concentration of TX and because washing after TX exposure restored similar tau2 IR both on immunohistochemistry and immunoblot. These findings are explained if tau, modified after ischemia, undergoes a reversible conformational change on TX exposure. Because conformation at Ser101 of bovine tau is crucial for its affinity to tau2, this Ser-like conformation mimicked by its human counterpart Pro may represent pathological modification of tau shared by microglia around ischemic foci and NFTs. Relative resistance of tau2 epitope in NFTs to TX exposure suggests that tau woven into NFTs confers additional stability to this pathological modification on tau2 epitope. Susceptibility of tau2 epitope to TX, seen in these microglia, is shared with glial cytoplasmic inclusions and will show its conformational state to be different from that in NFTs. PMID:14730711

  20. 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}.

  1. 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 CNS—brain and spinal cord tissue, interstitial fluid, and CSF—while 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

  2. Regulation of alternative splicing of tau exon 10.

    PubMed

    Qian, Wei; Liu, Fei

    2014-04-01

    The neuronal microtubule-associated protein tau is abnormally hyperphosphorylated and aggregated into neurofibrillary tangles in the brains of individuals with Alzheimer's disease and related neurodegenerative disorders. The adult human brain expresses six isoforms of tau generated by alternative splicing of exons 2, 3, and 10 of its pre-mRNA. Exon 10 encodes the second microtubule-binding repeat of tau. Its alternative splicing produces tau isoforms with either three or four microtubule-binding repeats, termed 3R-tau and 4Rtau. In the normal adult human brain, the level of 3R-tau is approximately equal to that of 4R-tau. Several silent and intronic mutations of the tau gene associated with FTDP-17T (frontotemporal dementia with Parkinsonism linked to chromosome 17 and specifically characterized by tau pathology) only disrupt exon 10 splicing, but do not influence the primary sequence of the tau protein. Thus, abnormal exon 10 splicing is sufficient to cause neurodegeneration and dementia. Here, we review the regulation of tau exon 10 splicing by cis-elements and trans-factors and summarize all the mutations associated with FTDP-17T and related tauopathies. The findings suggest that correction of exon 10 splicing may be a potential target for tau exon 10 splicing-related tauopathies. PMID:24627328

  3. Estimation of Tau and Phosphorylated Tau181 in Serum of Alzheimer’s Disease and Mild Cognitive Impairment Patients

    PubMed Central

    Shekhar, Shashank; Kumar, Rahul; Rai, Nitish; Kumar, Vijay; Singh, Kusum; Upadhyay, Ashish Datt; Tripathi, Manjari; Dwivedi, Sadanand; Dey, Aparajit B.; Dey, Sharmistha

    2016-01-01

    The elevated level of cerebrospinal fluid (CSF) Tau and phosphorylated Tau181 (p-Tau181) proteins are well established hallmarks of Alzheimer’s disease (AD). Elevated level of p-Tau181 can differentiate AD from other neurodegenerative disease. However, the expression level of these proteins in serum of AD patient is not well set up. This study sought to evaluate the level of Tau and p-Tau181 in serum of AD, and mild cognitive impairment (MCI) patients for an alternative approach to establish protein-based markers by convenient way. Blood samples were collected from 39 AD patients, 37 MCI patients and 37 elderly individuals as controls. The levels of Tau and p-Tau181 in the serum of the different groups were measured by label free real time Surface Plasmon Resonance technology by using specific antibodies, and were further confirmed by the conventional western blot method. An appropriate statistical analysis, including Receiver Operating Characteristic (ROC), was performed. The concentrations of serum Tau and p-Tau181 were significantly higher (p<0.00001) in AD (Tau; 47.49±9.00ng/μL, p-Tau181; 0.161±0.04 ng/μL) compared to MCI (Tau; 39.26±7.78 ng/μL, p-Tau181; 0.135±0.02 ng/μL) and were further higher compared to elderly controls (Tau; 34.92±6.58 ng/μL, p-Tau181; 0.122±0.01 ng/ μL). A significant (p<0.0001) downhill correlation was found between Tau as well as p-Tau181 levels with HMSE and MoCA score. This study for the first time reports the concentration of Tau and p-Tau181 in serum of AD and MCI patients. The cutoff values of Tau and p-Tau181 of AD and MCI patients with sensitivity and specificity reveal that serum level of these proteins can be used as a predictive marker for AD and MCI. PMID:27459603

  4. Detection of tau neutrinos by imaging air Cherenkov telescopes

    NASA Astrophysics Data System (ADS)

    Góra, D.; Bernardini, E.

    2016-09-01

    This paper investigates the potential to detect tau neutrinos in the energy range of 1-1000 PeV searching for very inclined showers with imaging Cherenkov telescopes. A neutrino induced tau lepton escaping from the Earth may decay and initiate an air shower which can be detected by a fluorescence or Cherenkov telescope. We present here a study of the detection potential of Earth-skimming neutrinos taking into account neutrino interactions in the Earth crust, local matter distributions at various detector sites, the development of tau-induced showers in air and the detection of Cherenkov photons with IACTs. We analyzed simulated shower images on the camera focal plane and implemented generic reconstruction chains based on Hillas parameters. We find that present IACTs can distinguish air showers induced by tau neutrinos from the background of hadronic showers in the PeV-EeV energy range. We present the neutrino trigger efficiency obtained for a few configurations being considered for the next-generation Cherenkov telescopes, i.e. the Cherenkov Telescope Array. Finally, for a few representative neutrino spectra expected from astrophysical sources, we compare the expected event rates at running IACTs to what is expected for the dedicated IceCube neutrino telescope.

  5. 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

  6. Trans-cellular propagation of Tau aggregation by fibrillar species.

    PubMed

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

    2012-06-01

    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

  7. Resolved multifrequency radio observations of GG Tau

    SciTech Connect

    Andrews, Sean M.; Birnstiel, T.; Rosenfeld, K. A.; Wilner, D. J.; Chandler, Claire J.; Pérez, 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.

  8. Selection of tau leptons with the CDF Run 2 trigger system

    SciTech Connect

    A. Anastassov; S. Baroiant; M. Chertok

    2003-07-01

    We have implemented triggers for hadronically decaying tau leptons within a framework of the CDF Run 2 trigger system. We describe the triggers, along with their physics motivations, and report on their initial performance.

  9. 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

  10. Phosphorylation of tau by glycogen synthase kinase 3beta affects the ability of tau to promote microtubule self-assembly.

    PubMed Central

    Utton, M A; Vandecandelaere, A; Wagner, U; Reynolds, C H; Gibb, G M; Miller, C C; Bayley, P M; Anderton, B H

    1997-01-01

    To study the effects of phosphorylation by glycogen synthase kinase-3beta (GSK-3beta) on the ability of the microtubule-associated protein tau to promote microtubule self-assembly, tau isoform 1 (foetal tau) and three mutant forms of this tau isoform were investigated. The three mutant forms of tau had the following serine residues, known to be phosphorylated by GSK-3, replaced with alanine residues so as to preclude their phosphorylation: (1) Ser-199 and Ser-202 (Ser-199/202-->Ala), (2) Ser-235 (Ser-235-->Ala) and (3) Ser-396 and Ser-404 (Ser-396/404-->Ala). Wild-type tau and the mutant forms of tau were phosphorylated with GSK-3beta, and their ability to promote microtubule self-assembly was compared with the corresponding non-phosphorylated tau species. In the non-phosphorylated form, wild-type tau and all of the mutants affected the mean microtubule length and number concentrations of assembled microtubules in a manner consistant with enhanced microtubule nucleation. Phosphorylation of these tau species with GSK-3beta consistently reduced the ability of a given tau species to promote microtubule self-assembly, although the affinity of the tau for the microtubules was not greatly affected by phosphorylation since the tau species remained largely associated with the microtubules. This suggests that the regulation of microtubule assembly can be controlled by phosphorylation of tau at sites accessible to GSK-3beta by a mechanism that does not necessarily involve the dissociation of tau from the microtubules. PMID:9169608

  11. Evidence for two distinct binding sites for tau on microtubules

    PubMed Central

    Makrides, Victoria; Massie, Michelle R.; Feinstein, Stuart C.; Lew, John

    2004-01-01

    The microtubule-associated protein tau regulates diverse and essential microtubule functions, from the nucleation and promotion of microtubule polymerization to the regulation of microtubule polarity and dynamics, as well as the spacing and bundling of axonal microtubules. Thermodynamic studies show that tau interacts with microtubules in the low- to mid-nanomolar range, implying moderate binding affinity. At the same time, it is well established that microtubule-bound tau does not undergo exchange with the bulk medium readily, suggesting that the tau-microtubule interaction is essentially irreversible. Given this dilemma, we investigated the mechanism of interaction between tau and microtubules in kinetic detail. Stopped-flow kinetic analysis reveals moderate binding affinity between tau and preassembled microtubules and rapid dissociation/association kinetics. In contrast, when microtubules are generated by copolymerization of tubulin and tau, a distinct population of microtubule-bound tau is observed, the binding of which seems irreversible. We propose that reversible binding occurs between tau and the surface of preassembled microtubules, whereas irreversible binding results when tau is coassembled with tubulin into a tau-microtubule copolymer. Because the latter is expected to be physiologically relevant, its characterization is of central importance. PMID:15096589

  12. 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.

  13. 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.

  14. Dimer model for Tau proteins bound in microtubule bundles

    NASA Astrophysics Data System (ADS)

    Hall, Natalie; Kluber, Alexander; Hayre, N. Robert; Singh, Rajiv; Cox, Daniel

    2013-03-01

    The microtubule associated protein tau is important in nucleating and maintaining microtubule spacing and structure in neuronal axons. Modification of tau is implicated as a later stage process in Alzheimer's disease, but little is known about the structure of tau in microtubule bundles. We present preliminary work on a proposed model for tau dimers in microtubule bundles (dimers are the minimal units since there is one microtubule binding domain per tau). First, a model of tau monomer was created and its characteristics explored using implicit solvent molecular dynamics simulation. Multiple simulations yield a partially collapsed form with separate positively/negatively charged clumps, but which are a factor of two smaller than required by observed microtubule spacing. We argue that this will elongate in dimer form to lower electrostatic energy at a cost of entropic ``spring'' energy. We will present preliminary results on steered molecular dynamics runs on tau dimers to estimate the actual force constant. Supported by US NSF Grant DMR 1207624.

  15. APP metabolism regulates tau proteostasis in human cerebral cortex neurons.

    PubMed

    Moore, Steven; Evans, Lewis D B; Andersson, Therese; Portelius, Erik; Smith, James; Dias, Tatyana B; Saurat, Nathalie; McGlade, Amelia; Kirwan, Peter; Blennow, Kaj; Hardy, John; Zetterberg, Henrik; Livesey, Frederick J

    2015-05-01

    Accumulation of Aβ peptide fragments of the APP protein and neurofibrillary tangles of the microtubule-associated protein tau are the cellular hallmarks of Alzheimer's 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 Aβ 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 β-secretase and γ-secretase inhibition, as well as γ-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 Aβ signaling to neurons. PMID:25921538

  16. 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 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 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 tanß values down to 25 for Higgs boson masses below 170 GeV/c2.

  17. 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; Åsman, 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; Besançon, 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-Pérez, E; Carrasco-Lizarraga, M A; Casey, B C K; Castilla-Valdez, H; Chakrabarti, S; Chakraborty, D; Chan, K M; Chandra, A; Chen, G; Chevalier-Théry, 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; Déliot, 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; Grünendahl, S; Grünewald, 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; Jaffré, 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; Kurča, 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; Magaña-Villalba, R; Malik, S; Malyshev, V L; Maravin, Y; Martínez-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 Garzón, 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; Pétroff, 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; Sánchez-Hernández, 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; Söldner-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; Wang, M H L S; Warchol, J; Watts, G; Wayne, M; Weber, M; Welty-Rieger, L; White, A; Wicke, D; Williams, M R J; Wilson, G W; 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; Youn, S W; Yu, J; Zelitch, S; Zhao, T; Zhou, B; Zhu, J; Zielinski, M; Zieminska, D; Zivkovic, L

    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 tanβ. 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 tanβ values down to 25 for Higgs boson masses below 170 GeV/c(2). PMID:22026764

  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

    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

  19. 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).

  20. 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.

  1. 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

  2. Tau Monoclonal Antibody Generation Based on Humanized Yeast Models

    PubMed Central

    Rosseels, Joëlle; Van den Brande, Jeff; Violet, Marie; Jacobs, Dirk; Grognet, Pierre; Lopez, Juan; Huvent, Isabelle; Caldara, Marina; Swinnen, Erwin; Papegaey, Anthony; Caillierez, Raphaëlle; Buée-Scherrer, Valerie; Engelborghs, Sebastiaan; Lippens, Guy; Colin, Morvane; Buée, 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

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

    PubMed Central

    Janning, Dennis; Igaev, Maxim; Sündermann, Frederik; Brühmann, Jörg; Beutel, Oliver; Heinisch, Jürgen 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 GFP–tagged tubulin that, despite this rapid dynamics, tau is capable of regulating the tubulin–microtubule 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

  4. Balmer decrements of T Tau stars

    NASA Astrophysics Data System (ADS)

    Katysheva, N. A.

    1981-04-01

    The relative intensities of Balmer lines calculated on the basis of Sobolev's probability method (1947) and the observed decrements of T Tau stars in the catalog of Cohen and Kuhi (1979) are compared with spectral classes between K5 and M5. For the group of stars, G5-K5, studied by Grinin (1980), emission was found to be predominantly of an envelope type, with less of a part played by chromospheric radiation. In K5-M5 stars, however, the envelope makes a smaller contribution to the total radiation, and most of the emission arises in the dense gas at the surface of the star. A comparison of the Balmer decrements of T Tau stars of different spectral classes and flare stars shows that in a transition to stars of lower luminosity, the role of chromospheric radiation increases.

  5. Can numerical modeling help understand the fate of tau protein in the axon terminal?

    PubMed

    Kuznetsov, I A; Kuznetsov, A V

    2016-01-01

    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

  6. 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 1–331) of human tau-tubulin kinase 2 was expressed in insect cells, purified and crystallized. Diffraction data have been collected to 2.9 Å 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 1–331) 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 Å, α = β = γ = 90.0°. Diffraction data were collected to 2.9 Å resolution using synchrotron radiation at BL24XU of SPring-8.

  7. 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.

  8. TAU as Tao. [interstellar spacecraft performance

    NASA Technical Reports Server (NTRS)

    Lyman, P. T.; Reid, M. S.

    1989-01-01

    This paper discusses the feasibility of building and launching a truly deep-space spacecraft mission that will penetrate near interstellar space to a depth of one thousand astronomical units (TAU) within a flight time of 50 years. Particular attention is given to the mission profile and to its communications system, power system, and propulsion system. Results of experimental studies indicate that, with advanced technology, reasonable trip times can be achieved and adequate science information can be brought to earth.

  9. Hyperphosphorylation results in tau dysfunction in DNA folding and protection.

    PubMed

    Lu, Yang; He, Hai-Jin; Zhou, Jun; Miao, Jun-Ye; Lu, Jing; He, Ying-Ge; Pan, Rong; Wei, Yan; Liu, Ying; He, Rong-Qiao

    2013-01-01

    Hyperphosphorylation of tau occurs in preclinical and clinical stages of Alzheimer's disease (AD), and hyperphosphorylated tau is the main constituent of the paired helical filaments in the brains of mild cognitive impairment and AD patients. While most of the work described so far focused on the relationship between hyperphosphorylation of tau and microtubule disassembly as well as axonal transport impairments, both phenomena ultimately leading to cell death, little work has been done to study the correlation between tau hyperphosphorylation and DNA damage. As we showed in this study, tau hyperphosphorylation and DNA damage co-occurred under formaldehyde treatment in N2a cells, indicating that phosphorylated tau (p-Tau) induced by formaldehyde may be involved in DNA impairment. After phosphorylation, the effect of tau in preventing DNA from thermal denaturation was diminished, its ability to accelerate DNA renaturation was lost, and its function in protecting DNA from reactive oxygen species (ROS) attack was impaired. Thus, p-Tau is not only associated with the disassembly of the microtubule system, but also plays a crucial role in DNA impairment. Hyperphosphorylation-mediated dysfunction of tau protein in prevention of DNA structure from damage under the attack of ROS may provide novel insights into the mechanisms underlying tauopathies. PMID:24064506

  10. The tau lepton in general relativity

    SciTech Connect

    Nienart, L.

    1988-01-01

    This dissertation presents the results of an investigation into trying to see how the mass of the tau lepton can arise from general Relativistic considerations. The formalism was applied earlier to electrons and predicted both the electron's mass and the muon's mass. The tau leptons mass will be found by considering the contribution of a non-zero magnetic moment to the quaternion fields and the spin affine connection fields in a Riemannian space. The exact mass operator is constructed from these fields, and is then approximated in 3 different ways in order to permit calculation. The expectation value of these approximations to the mass operator is then found, using the relativistic Coulomb wavefunctions. The choice of Coulomb states is due to the consideration that the pairs that comprise the vacuum in this field theory couple to the magnetic moment of the core electron in a manner resembling that of the electrons in the Hydrogen atom. As the coupling the author is considering in his model is that of magnetic dipole by design, an argument is presented in which the Coulombic coupling strength parameters of the Coulomb states are scaled in order to provide a suitable description of the magnetic states which the author is actually interested in. The resulting values for the mass of the tau lepton are then within half an order of magnitude of the experimental values.

  11. 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; Sepčić, 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 (0.5 µg/ml) and hTau (1 µg/ml; ~22 µM) 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; 1 nM, 24 h). 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 (0.005 µg/ml) and hTau (1 µg/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 (1.2 nM) intrahippocampally. When tested 2 weeks 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

  12. 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.

  13. 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.

  14. Tau protein is essential for stress-induced brain pathology.

    PubMed

    Lopes, Sofia; Vaz-Silva, João; Pinto, Vitor; Dalla, Christina; Kokras, Nikolaos; Bedenk, Benedikt; Mack, Natalie; Czisch, Michael; Almeida, Osborne F X; Sousa, Nuno; Sotiropoulos, Ioannis

    2016-06-28

    Exposure to chronic stress is frequently accompanied by cognitive and affective disorders in association with neurostructural adaptations. Chronic stress was previously shown to trigger Alzheimer's-like neuropathology, which is characterized by Tau hyperphosphorylation and missorting into dendritic spines followed by memory deficits. Here, we demonstrate that stress-driven hippocampal deficits in wild-type mice are accompanied by synaptic missorting of Tau and enhanced Fyn/GluN2B-driven synaptic signaling. In contrast, mice lacking Tau [Tau knockout (Tau-KO) mice] do not exhibit stress-induced pathological behaviors and atrophy of hippocampal dendrites or deficits of hippocampal connectivity. These findings implicate Tau as an essential mediator of the adverse effects of stress on brain structure and function. PMID:27274066

  15. 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

  16. Tau reconstruction methods at an electron-positron collider in the search for new physics

    NASA Astrophysics Data System (ADS)

    Li, Jinmian; Williams, Anthony G.

    2016-04-01

    By exploiting the relatively long lifetime of the tau lepton, we propose several novel methods for searching for new physics at an electron-positron collider. We consider processes that involve final states consisting of a tau lepton pair plus two missing particles. The mass and spin of the new physics particles can be measured in 3-prong tau decays. The tau polarization, which reflects the coupling to new physics, can be measured from the τ →π ν decay channel using the impact parameter distribution of the charged pion. We also discuss the corresponding backgrounds for these measurements, the next-to-leading order (NLO) effects, and the implications of finite detector resolution.

  17. Waring's problem with the Ramanujan \\tau-function

    NASA Astrophysics Data System (ADS)

    Garaev, M. Z.; Garcia, V. C.; Konyagin, S. V.

    2008-02-01

    We prove that for every integer N the Diophantine equation \\sum_{i=1}^{74000}\\tau(n_i)=N, where \\tau(n) is the Ramanujan \\tau-function, has a solution in positive integers n_1, n_2,\\dots, n_{74000} satisfying the condition \\max_{1\\le i\\le 74000}n_i\\,{\\ll}\\vert N\\vert^{2/11}+1. We also consider similar questions in residue fields modulo a large prime p.

  18. Temperature and toxic Tau in Alzheimer's disease: new insights

    PubMed Central

    Carrettiero, Daniel Carneiro; Santiago, Fernando Enrique; Motzko-Soares, Anna Carolina Parracho; Almeida, Maria Camila

    2015-01-01

    Alzheimer's disease (AD), the most common dementia in the elderly, is characterized by cognitive impairment and severe autonomic symptoms such as disturbance in core body temperature (Tc), which may be predictors or early events in AD onset. Inclusions of phosphorylated Tau (p-Tau) are a hallmark of AD and other neurodegenerative disorders called “Tauopathies.” Animal and human studies show that anesthesia augments p-Tau levels through reduction of Tc, with implications for AD. Additionally, hypothermia impairs memory and cognitive function. The molecular networks related to Tc that are associated with AD remain poorly characterized. Under physiological conditions, Tau binds microtubules, promoting their assembly and stability. The dynamically regulated Tau-microtubule interaction plays an important role in structural remodeling of the cytoskeleton, having important functions in neuronal plasticity and memory in the hippocampus. Hypothermia-induced increases in p-Tau levels are significant, with an 80% increase for each degree Celsius below normothermic conditions. Although the effects of temperature on Tau phosphorylation are evident, its effects on p-Tau degradation remain poorly understoodWe review information concerning the mechanisms of Tau regulation of neuron plasticity via its effects on microtubule dynamics, with focus on pathways regulating the abundance of phosphorylated Tau species.  We highlight the effects of temperature on molecular mechanisms influencing the development of Tau-related diseases. Specifically, we argue that cold might preferentially affects central nervous system structures that are highly reliant upon plasticity, such as the hippocampus, and that the effect of cold on Tau phosphorylation may constitute a pathology-initiating trigger leading to neurodegeneration. PMID:27227069

  19. 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

  20. MSUT2 is a determinant of susceptibility to tau neurotoxicity.

    PubMed

    Guthrie, Chris R; Greenup, Lynne; Leverenz, James B; Kraemer, Brian C

    2011-05-15

    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

  1. 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

  2. CHIP and Hsp70 regulate tau ubiquitination, degradation and aggregation.

    PubMed

    Petrucelli, Leonard; Dickson, Dennis; Kehoe, Kathryn; Taylor, Julie; Snyder, Heather; Grover, Andrew; De Lucia, Michael; McGowan, Eileen; Lewis, Jada; Prihar, Guy; Kim, Jungsu; Dillmann, Wolfgang H; Browne, Susan E; Hall, Alexis; Voellmy, Richard; Tsuboi, Yoshio; Dawson, Ted M; Wolozin, Benjamin; Hardy, John; Hutton, Mike

    2004-04-01

    Molecular chaperones, ubiquitin ligases and proteasome impairment have been implicated in several neurodegenerative diseases, including Alzheimer's and Parkinson's disease, which are characterized by accumulation of abnormal protein aggregates (e.g. tau and alpha-synuclein respectively). Here we report that CHIP, an ubiquitin ligase that interacts directly with Hsp70/90, induces ubiquitination of the microtubule associated protein, tau. CHIP also increases tau aggregation. Consistent with this observation, diverse of tau lesions in human postmortem tissue were found to be immunopositive for CHIP. Conversely, induction of Hsp70 through treatment with either geldanamycin or heat shock factor 1 leads to a decrease in tau steady-state levels and a selective reduction in detergent insoluble tau. Furthermore, 30-month-old mice overexpressing inducible Hsp70 show a significant reduction in tau levels. Together these data demonstrate that the Hsp70/CHIP chaperone system plays an important role in the regulation of tau turnover and the selective elimination of abnormal tau species. Hsp70/CHIP may therefore play an important role in the pathogenesis of tauopathies and also represents a potential therapeutic target. PMID:14962978

  3. Cellular factors modulating the mechanism of tau protein aggregation.

    PubMed

    Fontaine, Sarah N; Sabbagh, Jonathan J; Baker, Jeremy; Martinez-Licha, Carlos R; Darling, April; Dickey, Chad A

    2015-05-01

    Pathological accumulation of the microtubule-associated protein tau, in the form of neurofibrillary tangles, is a major hallmark of Alzheimer's disease, the most prevalent neurodegenerative condition worldwide. In addition to Alzheimer's disease, a number of neurodegenerative diseases, called tauopathies, are characterized by the accumulation of aggregated tau in a variety of brain regions. While tau normally plays an important role in stabilizing the microtubule network of the cytoskeleton, its dissociation from microtubules and eventual aggregation into pathological deposits is an area of intense focus for therapeutic development. Here we discuss the known cellular factors that affect tau aggregation, from post-translational modifications to molecular chaperones. PMID:25666877

  4. Tau Mislocation in Glucocorticoid-Triggered Hippocampal Pathology.

    PubMed

    Pinheiro, Sara; Silva, Joana; Mota, Cristina; Vaz-Silva, João; Veloso, Ana; Pinto, Vítor; Sousa, Nuno; Cerqueira, João; Sotiropoulos, Ioannis

    2016-09-01

    The exposure to high glucocorticoids (GC) triggers neuronal atrophy and cognitive deficits, but the exact cellular mechanisms underlying the GC-associated dendritic remodeling and spine loss are still poorly understood. Previous studies have implicated sustained GC elevations in neurodegenerative mechanisms through GC-evoked hyperphosphorylation of the cytoskeletal protein Tau while Tau mislocation has recently been proposed as relevant in Alzheimer's disease (AD) pathology. In light of the dual cytoplasmic and synaptic role of Tau, this study monitored the impact of prolonged GC treatment on Tau intracellular localization and its phosphorylation status in different cellular compartments. We demonstrate, both by biochemical and ultrastructural analysis, that GC administration led to cytosolic and dendritic Tau accumulation in rat hippocampus, and triggered Tau hyperphosphorylation in epitopes related to its malfunction (Ser396/404) and cytoskeletal pathology (e.g., Thr231 and Ser262). In addition, we show, for the first time, that chronic GC administration also increased Tau levels in synaptic compartment; however, at the synapse, there was an increase in phosphorylation of Ser396/404, but a decrease of Thr231. These GC-triggered Tau changes were paralleled by reduced levels of synaptic scaffolding proteins such as PSD-95 and Shank proteins as well as reduced dendritic branching and spine loss. These in vivo findings add to our limited knowledge about the underlying mechanisms of GC-evoked synaptic atrophy and neuronal disconnection implicating Tau missorting in mechanism(s) of synaptic damage, beyond AD pathology. PMID:26328538

  5. NMR Meets Tau: Insights into Its Function and Pathology

    PubMed Central

    Lippens, Guy; Landrieu, Isabelle; Smet, Caroline; Huvent, Isabelle; Gandhi, Neha S.; Gigant, Benoît; Despres, Clément; Qi, Haoling; Lopez, Juan

    2016-01-01

    In this review, we focus on what we have learned from Nuclear Magnetic Resonance (NMR) studies on the neuronal microtubule-associated protein Tau. We consider both the mechanistic details of Tau: the tubulin relationship and its aggregation process. Phosphorylation of Tau is intimately linked to both aspects. NMR spectroscopy has depicted accurate phosphorylation patterns by different kinases, and its non-destructive character has allowed functional assays with the same samples. Finally, we will discuss other post-translational modifications of Tau and its interaction with other cellular factors in relationship to its (dys)function. PMID:27338491

  6. Tau physiology and pathomechanisms in frontotemporal lobar degeneration.

    PubMed

    Bodea, Liviu-Gabriel; Eckert, Anne; Ittner, Lars Matthias; Piguet, Olivier; Götz, Jürgen

    2016-08-01

    Frontotemporal lobar degeneration (FTLD) has been associated with toxic intracellular aggregates of hyperphosphorylated tau (FTLD-tau). Moreover, genetic studies identified mutations in the MAPT gene encoding tau in familial cases of the disease. In this review, we cover a range of aspects of tau function, both in the healthy and diseased brain, discussing several in vitro and in vivo models. Tau structure and function in the healthy brain is presented, accentuating its distinct compartmentalization in neurons and its role in microtubule stabilization and axonal transport. Furthermore, tau-driven pathology is discussed, introducing current concepts and the underlying experimental evidence. Different aspects of pathological tau phosphorylation, the protein's genomic and domain organization as well as its spreading in disease, together with MAPT-associated mutations and their respective models are presented. Dysfunction related to other post-transcriptional modifications and their effect on normal neuronal functions such as cell cycle, epigenetics and synapse dynamics are also discussed, providing a mechanistic explanation for the observations made in FTLD-tau cases, with the possibility for therapeutic intervention. In this review, we cover aspects of tau function, both in the healthy and diseased brain, referring to different in vitro and in vivo models. In healthy neurons, tau is compartmentalized, with higher concentrations found in the distal part of the axon. Cargo molecules are sensitive to this gradient. A disturbed tau distribution, as found in frontotemporal lobar degeneration (FTLD-tau), has severe consequences for cellular physiology: tau accumulates in the neuronal soma and dendrites, leading among others to microtubule depolymerization and impaired axonal transport. Tau forms insoluble aggregates that sequester additional molecules stalling cellular physiology. Neuronal communication is gradually lost as toxic tau accumulates in dendritic spines

  7. Cellular factors modulating the mechanism of tau protein aggregation

    PubMed Central

    Fontaine, Sarah N.; Sabbagh, Jonathan J.; Baker, Jeremy; Martinez-Licha, Carlos R.; Darling, April

    2015-01-01

    Pathological accumulation of the microtubule-associated protein tau, in the form of neurofibrillary tangles, is a major hallmark of Alzheimer’s disease, the most prevalent neurodegenerative condition worldwide. In addition to Alzheimer’s disease, a number of neurodegenerative diseases, called tauopathies, are characterized by the accumulation of aggregated tau in a variety of brain regions. While tau normally plays an important role in stabilizing the microtubule network of the cytoskeleton, its dissociation from microtubules and eventual aggregation into pathological deposits is an area of intense focus for therapeutic development. Here we discuss the known cellular factors that affect tau aggregation, from post-translational modifications to molecular chaperones. PMID:25666877

  8. Connecting the Dots Between Tau Dysfunction and Neurodegeneration

    PubMed Central

    Frost, Bess; Götz, Jürgen; Feany, Mel B.

    2014-01-01

    Tauopathies are devastating and ultimately fatal neurodegenerative diseases, which are histopathologically defined by insoluble filamentous deposits of abnormally phosphorylated tau protein within neurons and glia. Identifying the causes of abnormal tau phosphorylation and subsequent aggregation has been the focus of much research, and is currently a major target for the development of therapeutic interventions for tauopathies, including Alzheimer’s disease. Recently much has been learned about the sequence of events that lead from tau dysfunction to neuronal death. This review focuses on the cascade of events that are catalyzed by pathological tau, and highlights current and potential therapeutic strategies to target this pathway. PMID:25172552

  9. 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

  10. NMR Meets Tau: Insights into Its Function and Pathology.

    PubMed

    Lippens, Guy; Landrieu, Isabelle; Smet, Caroline; Huvent, Isabelle; Gandhi, Neha S; Gigant, Benoît; Despres, Clément; Qi, Haoling; Lopez, Juan

    2016-01-01

    In this review, we focus on what we have learned from Nuclear Magnetic Resonance (NMR) studies on the neuronal microtubule-associated protein Tau. We consider both the mechanistic details of Tau: the tubulin relationship and its aggregation process. Phosphorylation of Tau is intimately linked to both aspects. NMR spectroscopy has depicted accurate phosphorylation patterns by different kinases, and its non-destructive character has allowed functional assays with the same samples. Finally, we will discuss other post-translational modifications of Tau and its interaction with other cellular factors in relationship to its (dys)function. PMID:27338491

  11. 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

  12. Stabilization of Microtubule-Unbound Tau via Tau Phosphorylation at Ser262/356 by Par-1/MARK Contributes to Augmentation of AD-Related Phosphorylation and Aβ42-Induced Tau Toxicity

    PubMed Central

    Ando, Kanae; Maruko-Otake, Akiko; Ohtake, Yosuke; Hayashishita, Motoki; Sekiya, Michiko; Iijima, Koichi M.

    2016-01-01

    Abnormal accumulation of the microtubule-interacting protein tau is associated with neurodegenerative diseases including Alzheimer’s disease (AD). β-amyloid (Aβ) lies upstream of abnormal tau behavior, including detachment from microtubules, phosphorylation at several disease-specific sites, and self-aggregation into toxic tau species in AD brains. To prevent the cascade of events leading to neurodegeneration in AD, it is essential to elucidate the mechanisms underlying the initial events of tau mismetabolism. Currently, however, these mechanisms remain unclear. In this study, using transgenic Drosophila co-expressing human tau and Aβ, we found that tau phosphorylation at AD-related Ser262/356 stabilized microtubule-unbound tau in the early phase of tau mismetabolism, leading to neurodegeneration. Aβ increased the level of tau detached from microtubules, independent of the phosphorylation status at GSK3-targeted SP/TP sites. Such mislocalized tau proteins, especially the less phosphorylated species, were stabilized by phosphorylation at Ser262/356 via PAR-1/MARK. Levels of Ser262 phosphorylation were increased by Aβ42, and blocking this stabilization of tau suppressed Aβ42-mediated augmentation of tau toxicity and an increase in the levels of tau phosphorylation at the SP/TP site Thr231, suggesting that this process may be involved in AD pathogenesis. In contrast to PAR-1/MARK, blocking tau phosphorylation at SP/TP sites by knockdown of Sgg/GSK3 did not reduce tau levels, suppress tau mislocalization to the cytosol, or diminish Aβ-mediated augmentation of tau toxicity. These results suggest that stabilization of microtubule-unbound tau by phosphorylation at Ser262/356 via the PAR-1/MARK may act in the initial steps of tau mismetabolism in AD pathogenesis, and that such tau species may represent a potential therapeutic target for AD. PMID:27023670

  13. 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.

  14. 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.

  15. Mobility and subcellular localization of endogenous, gene-edited Tau differs from that of over-expressed human wild-type and P301L mutant Tau

    PubMed Central

    Di Xia; Gutmann, Julia M.; Götz, Jürgen

    2016-01-01

    Alzheimer’s disease (AD) and a subset of frontotemporal dementia termed FTLD-Tau are characterized by a massive, yet incompletely characterized and understood redistribution of Tau. To establish a framework for understanding this pathology, we used the genome-editing tool TALEN and generated Tau-mEOS2 knock-in mice to determine the mobility and subcellular localization of endogenous Tau in hippocampal cultures. We analysed Tau in axons, dendrites and spines at three stages of maturation using live-cell imaging, photo-conversion and FRAP assays. Tau-mEOS2 cultures were compared with those over-expressing EGFP-tagged forms of human wild-type (hWT-Tau) and P301L mutant Tau (hP301L-Tau), modelling Tau accumulation in AD and FTLD-Tau, respectively. In developing neurons, Tau-mEOS2 followed a proximo-distal gradient in axons and a subcellular distribution similar to that of endogenous Tau in neurons obtained from wild-type mice, which were abolished, when either hWT-Tau or hP301L-Tau was over-expressed. For the three conditions, FRAP analysis revealed a similar mobility in dendrites compared with axons; however, Tau-mEOS2 was less mobile than hWT-Tau and hP301L-Tau and the mobile fraction was smaller, possibly reflecting less efficient microtubule binding of Tau when over-expressed. Together, our study presents Tau-mEOS2 mice as a novel tool for the study of Tau in a physiological and a pathological context. PMID:27378256

  16. Mobility and subcellular localization of endogenous, gene-edited Tau differs from that of over-expressed human wild-type and P301L mutant Tau.

    PubMed

    Di Xia; Gutmann, Julia M; Götz, Jürgen

    2016-01-01

    Alzheimer's disease (AD) and a subset of frontotemporal dementia termed FTLD-Tau are characterized by a massive, yet incompletely characterized and understood redistribution of Tau. To establish a framework for understanding this pathology, we used the genome-editing tool TALEN and generated Tau-mEOS2 knock-in mice to determine the mobility and subcellular localization of endogenous Tau in hippocampal cultures. We analysed Tau in axons, dendrites and spines at three stages of maturation using live-cell imaging, photo-conversion and FRAP assays. Tau-mEOS2 cultures were compared with those over-expressing EGFP-tagged forms of human wild-type (hWT-Tau) and P301L mutant Tau (hP301L-Tau), modelling Tau accumulation in AD and FTLD-Tau, respectively. In developing neurons, Tau-mEOS2 followed a proximo-distal gradient in axons and a subcellular distribution similar to that of endogenous Tau in neurons obtained from wild-type mice, which were abolished, when either hWT-Tau or hP301L-Tau was over-expressed. For the three conditions, FRAP analysis revealed a similar mobility in dendrites compared with axons; however, Tau-mEOS2 was less mobile than hWT-Tau and hP301L-Tau and the mobile fraction was smaller, possibly reflecting less efficient microtubule binding of Tau when over-expressed. Together, our study presents Tau-mEOS2 mice as a novel tool for the study of Tau in a physiological and a pathological context. PMID:27378256

  17. 18F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers

    PubMed Central

    Puschmann, Andreas; Schöll, Michael; Ohlsson, Tomas; van Swieten, John; Honer, Michael; Englund, Elisabet

    2016-01-01

    Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo. However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with 18F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer’s disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited 18F-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was 18F-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-β (18F-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that 18F-AV-1451 positron emission tomography can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein. PMID:27357347

  18. 18F-AV-1451 tau PET imaging correlates strongly with tau neuropathology in MAPT mutation carriers.

    PubMed

    Smith, Ruben; Puschmann, Andreas; Schöll, Michael; Ohlsson, Tomas; van Swieten, John; Honer, Michael; Englund, Elisabet; Hansson, Oskar

    2016-09-01

    Tau positron emission tomography ligands provide the novel possibility to image tau pathology in vivo However, little is known about how in vivo brain uptake of tau positron emission tomography ligands relates to tau aggregates observed post-mortem. We performed tau positron emission tomography imaging with (18)F-AV-1451 in three patients harbouring a p.R406W mutation in the MAPT gene, encoding tau. This mutation results in 3- and 4-repeat tau aggregates similar to those in Alzheimer's disease, and many of the mutation carriers initially suffer from memory impairment and temporal lobe atrophy. Two patients with short disease duration and isolated memory impairment exhibited (18)F-AV-1451 uptake mainly in the hippocampus and adjacent temporal lobe regions, correlating with glucose hypometabolism in corresponding regions. One patient died after 26 years of disease duration with dementia and behavioural deficits. Pre-mortem, there was (18)F-AV-1451 uptake in the temporal and frontal lobes, as well as in the basal ganglia, which strongly correlated with the regional extent and amount of tau pathology in post-mortem brain sections. Amyloid-β ((18)F-flutemetamol) positron emission tomography scans were negative in all cases, as were stainings of brain sections for amyloid. This provides strong evidence that (18)F-AV-1451 positron emission tomography can be used to accurately quantify in vivo the regional distribution of hyperphosphorylated tau protein. PMID:27357347

  19. Truncation of tau at E391 Promotes Early Pathological Changes in Transgenic Mice

    PubMed Central

    McMillan, Pamela J.; Kraemer, Brian C.; Robinson, Linda; Leverenz, James B.; Raskind, Murray; Schellenberg, Gerard

    2011-01-01

    Proteolytic cleavage of tau at glutamic acid 391 (E391) is linked to the pathogenesis of Alzheimer disease (AD). This C-terminal truncated tau species exists in neurofibrillary tangles and abnormal neurites in the brains of AD patients and may potentiate tau polymerization. We generated a mouse model that expresses human tau truncated at E391 to begin to elucidate the role of this C-terminal truncated tau species in the development of tau pathology. Our results show that truncated but otherwise wild type human tau is sufficient to drive pre-tangle pathological changes in tau, including accumulation of insoluble tau, somatodendritic redistribution, formation of pathological conformations, and dual phosphorylation of tau at sites associated with AD pathology. In addition, these mice exhibit atypical neuritic tau immunoreactivity, including abnormal neuritic processes and dystrophic neurites. These results suggest that changes in tau proteolysis can initiate tauopathy. PMID:22002427

  20. Sequestration of tau by granulovacuolar degeneration in Alzheimer's disease.

    PubMed Central

    Bondareff, W.; Wischik, C. M.; Novak, M.; Roth, M.

    1991-01-01

    Antibodies directed against three regions of tau have been used in a histologic study of granulovacuolar degeneration (GVD) in Alzheimer's disease (AD). Granulovascular degeneration complexes, consisting of a dense granule in a less-dense vacuole, were found in hippocampal pyramidal neurons in all patients studied. Anti-tau antibodies directed against the N-and C-termini, and the repeat region of tau, were found to immunolabel the granule of the GVD complex. Intracellular neurofibrillary tangles also were labeled by these antibodies. In particular, MAb6.423, which recognizes tau protein sequestered in paired helical filaments (PHF) in AD, but not the normal tau proteins so far described in human brain, labeled GVD granules. Contrarily, a generic tau marker (MAb7.51), which immunolabels all known isoforms of isolated and expressed tau protein, including PHF-tau, did not label the GVD granule. These findings demonstrate that the entire tau molecule is sequestered within the GVD granule, and that the tau protein found in GVD complexes is antigenically related to that found in PHFs. There is, however, a difference in the way in which the repeat region of tau is incorporated into the two structures, making the MAb7.51 epitope unavailable in the GVD complex. These findings suggest that the formation of GVD complexes in hippocampal pyramidal neurons vulnerable to neurofibrillary degeneration may represent an alternative pathway for dealing with an aberrant molecular complex, which contributes to the formation of GVD granules and neurofibrillary tangles in AD. Images Figure 1 PMID:1909492

  1. nu. sub. mu. and. nu. sub. tau. as dark matter

    SciTech Connect

    Carlson, E.D.; Hall, L.J. )

    1989-11-15

    The singlet-Majoron model, with {ital B}{minus}{ital L} broken spontaneously at the GeV scale, allows {Omega}=1 in {nu}{sub {mu}} or {nu}{sub {tau}} with masses in the range of 1 keV to 35 MeV. Neutrino-Majoron scattering leads to an unusual processing of the density perturbation spectrum; the resulting large-scale structure will be very similar to warm or cold dark matter. The Higgs boson may decay predominantly into invisible channels giving signatures with a missing-mass peak.

  2. Microtubule-associated protein tau (tau) is a major antigenic component of paired helical filaments in Alzheimer disease.

    PubMed Central

    Kosik, K S; Joachim, C L; Selkoe, D J

    1986-01-01

    The detailed protein composition of the paired helical filaments (PHF) that accumulate in human neurons in aging and Alzheimer disease is unknown. However, the identity of certain components has been surmised by using immunocytochemical techniques. Whereas PHF share epitopes with neurofilament proteins and microtubule-associated protein (MAP) 2, we report evidence that the MAP tau (tau) appears to be their major antigenic component. Immunization of rabbits with NaDodSO4-extracted, partially purified PHF (free of normal cytoskeletal elements, including tau) consistently produces antibodies to tau but not, for example, to neurofilaments. Such PHF antibodies label all of the heterogeneous fetal and mature forms of tau from rat and human brain. Absorption of PHF antisera with heat-stable MAPs (rich in tau) results in almost complete loss of staining of neurofibrillary tangles (NFT) in human brain sections. An affinity-purified antibody to tau specifically labels NFT and the neurites of senile plaques in human brain sections as well as NaDodSO4-extracted NFT. tau-Immunoreactive NFT frequently extend into the apical dendrites of pyramidal neurons, suggesting an aberrant intracellular locus for this axonal protein. tau and PHF antibodies label tau proteins identically on electrophoretic transfer blots and stain the gel-excluded protein representing NaDodSO4-insoluble PHF in homogenates of human brain. The progressive accumulation of altered tau protein in neurons in Alzheimer disease may result in instability of microtubules, consequent loss of effective transport of molecules and organelles, and, ultimately, neuronal death. Images PMID:2424016

  3. The many faces of interferon tau.

    PubMed

    Bazer, Fuller W; Ying, Wei; Wang, Xiaoqiu; Dunlap, Kathrin A; Zhou, Beiyan; Johnson, Greg A; Wu, Guoyao

    2015-03-01

    Interferon tau (IFNT) was discovered as the pregnancy recognition signal in ruminants, but is now known to have a plethora of physiological functions in the mammalian uterus. The mammalian uterus includes, from the outer surface to the lumen, the serosa, myometrium and endometrium. The endometrium consists of the luminal, superficial glandular, and glandular epithelia, each with a unique phenotype, stromal cells, vascular elements, nerves and immune cells. The uterine epithelia secrete or selectively transport molecules into the uterine lumen that are collectively known as histotroph. Histotroph is required for growth and development of the conceptus (embryo and its associated extra-embryonic membranes) and includes nutrients such as amino acids and glucose, enzymes, growth factors, cytokines, lymphokines, transport proteins for vitamins and minerals and extracellular matrix molecules. Interferon tau and progesterone stimulate transport of amino acids in histotroph, particularly arginine. Arginine stimulates the mechanistic target of rapamycin pathway to induce proliferation, migration and protein synthesis by cells of the conceptus, and arginine is the substrate for synthesis of nitric oxide and polyamines required for growth and development of the conceptus. In ruminants, IFNT also acts in concert with progesterone from the corpus luteum to increase expression of genes for transport of nutrients into the uterine lumen, as well as proteases, protease inhibitors, growth factors for hematopoiesis and angiogenesis and other molecules critical for implantation and placentation. Collectively, the pleiotropic effects of IFNT contribute to survival, growth and development of the ruminant conceptus. PMID:25557050

  4. 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

  5. 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.

  6. Dimethyl Sulfoxide Induces Both Direct and Indirect Tau Hyperphosphorylation

    PubMed Central

    Julien, Carl; Marcouiller, François; Bretteville, Alexis; El Khoury, Noura B.; Baillargeon, Joanie; Hébert, Sébastien S.; Planel, Emmanuel

    2012-01-01

    Dimethyl sulfoxide (DMSO) is widely used as a solvent or vehicle for biological studies, and for treatment of specific disorders, including traumatic brain injury and several forms of amyloidosis. As Alzheimer’s disease (AD) brains are characterized by deposits of β-amyloid peptides, it has been suggested that DMSO could be used as a treatment for this devastating disease. AD brains are also characterized by aggregates of hyperphosphorylated tau protein, but the effect of DMSO on tau phosphorylation is unknown. We thus investigated the impact of DMSO on tau phosphorylation in vitro and in vivo. One hour following intraperitoneal administration of 1 or 2 ml/kg DMSO in mice, no change was observed in tau phosphorylation. However, at 4 ml/kg, tau was hyperphosphorylated at AT8 (Ser202/Thr205), PHF-1 (Ser396/Ser404) and AT180 (Thr231) epitopes. At this dose, we also noticed that the animals were hypothermic. When the mice were maintained normothermic, the effect of 4 ml/kg DMSO on tau hyperphosphorylation was prevented. On the other hand, in SH-SY5Y cells, 0.1% DMSO induced tau hyperphosphorylation at AT8 and AT180 phosphoepitopes in normothermic conditions. Globally, these findings demonstrate that DMSO can induce tau hyperphosphorylation indirectly via hypothermia in vivo, and directly in vitro. These data should caution researchers working with DMSO as it can induce artifactual results both in vivo and in vitro. PMID:22768202

  7. The tau and beyond: Future research on heavy leptons

    SciTech Connect

    Perl, M.I.

    1988-01-01

    This paper outlines directions for future experimental research on the tau and tau neutrino. Present limits on the existence of heavier charged leptons are reviewed, with emphasis on the close-mass lepton pair concept. 44 refs., 8 figs., 5 tabs.

  8. Tau co-organizes dynamic microtubule and actin networks

    PubMed Central

    Elie, Auréliane; Prezel, Elea; Guérin, 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

  9. What triggered the early planet formation processes in HL Tau?

    NASA Astrophysics Data System (ADS)

    Plevne, O.

    2016-06-01

    T Tauri stars are in the pre-main sequence phase of stellar evolution. These stars convert their own gravitational potential energy to light, but their cores do not have enough temperature for nuclear reactions like a main sequence star. T Tauri stars are surrounded by a circumstellar disk, hot plasma and dust. Some T Tauri stars host protoplanetary objects in their circumstellar disk such as HL Tau. In this case HL Tau system is a good example for stellar evolution and planet formation. But HL Tau's protoplanetary objects were formed earlier than planet formation theories' expectations. With this purpose, this study will discuss "What triggered the early planet formation processes in HL Tau system?" with XMM-Newton and Chandra observations of HL Tau system.

  10. 14-3-3ζ Mediates Tau Aggregation in Human Neuroblastoma M17 Cells

    PubMed Central

    Li, Tong; Paudel, Hemant K.

    2016-01-01

    Microtubule-associated protein tau is the major component of paired helical filaments (PHFs) associated with the neuropathology of Alzheimer’s disease (AD). Tau in the normal brain binds and stabilizes microtubules. Tau isolated from PHFs is hyperphosphorylated, which prevents it from binding to microtubules. Tau phosphorylation has been suggested to be involved in the development of NFT pathology in the AD brain. Recently, we showed that 14-3-3ζ is bound to tau in the PHFs and when incubated in vitro with 14-3-3ζ, tau formed amorphous aggregates, single-stranded straight filaments, double stranded ribbon-like filaments and PHF-like filaments that displayed close resemblance with corresponding ultrastructures of AD brain. Surprisingly however, phosphorylated and non-phosphorylated tau aggregated in a similar manner, indicating that tau phosphorylation does not affect in vitro tau aggregation (Qureshi et al (2013) Biochemistry 52, 6445–6455). In this study, we have examined the role of tau phosphorylation in tau aggregation in cellular level. We have found that in human M17 neuroblastoma cells, tau phosphorylation by GSK3β or PKA does not cause tau aggregation, but promotes 14-3-3ζ-induced tau aggregation by destabilizing microtubules. Microtubule disrupting drugs also promoted 14-3-3ζ-induced tau aggregation without changing tau phosphorylation in M17 cell. In vitro, when incubated with 14-3-3ζ and microtubules, nonphosphorylated tau bound to microtubules and did not aggregate. Phosphorylated tau on the other hand did not bind to microtubules and aggregated. Our data indicate that microtubule-bound tau is resistant to 14-3-3ζ-induced tau aggregation and suggest that tau phosphorylation promotes tau aggregation in the brain by detaching tau from microtubules and thus making it accessible to 14-3-3ζ. PMID:27548710

  11. 14-3-3ζ Mediates Tau Aggregation in Human Neuroblastoma M17 Cells.

    PubMed

    Li, Tong; Paudel, Hemant K

    2016-01-01

    Microtubule-associated protein tau is the major component of paired helical filaments (PHFs) associated with the neuropathology of Alzheimer's disease (AD). Tau in the normal brain binds and stabilizes microtubules. Tau isolated from PHFs is hyperphosphorylated, which prevents it from binding to microtubules. Tau phosphorylation has been suggested to be involved in the development of NFT pathology in the AD brain. Recently, we showed that 14-3-3ζ is bound to tau in the PHFs and when incubated in vitro with 14-3-3ζ, tau formed amorphous aggregates, single-stranded straight filaments, double stranded ribbon-like filaments and PHF-like filaments that displayed close resemblance with corresponding ultrastructures of AD brain. Surprisingly however, phosphorylated and non-phosphorylated tau aggregated in a similar manner, indicating that tau phosphorylation does not affect in vitro tau aggregation (Qureshi et al (2013) Biochemistry 52, 6445-6455). In this study, we have examined the role of tau phosphorylation in tau aggregation in cellular level. We have found that in human M17 neuroblastoma cells, tau phosphorylation by GSK3β or PKA does not cause tau aggregation, but promotes 14-3-3ζ-induced tau aggregation by destabilizing microtubules. Microtubule disrupting drugs also promoted 14-3-3ζ-induced tau aggregation without changing tau phosphorylation in M17 cell. In vitro, when incubated with 14-3-3ζ and microtubules, nonphosphorylated tau bound to microtubules and did not aggregate. Phosphorylated tau on the other hand did not bind to microtubules and aggregated. Our data indicate that microtubule-bound tau is resistant to 14-3-3ζ-induced tau aggregation and suggest that tau phosphorylation promotes tau aggregation in the brain by detaching tau from microtubules and thus making it accessible to 14-3-3ζ. PMID:27548710

  12. 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 (10 min) enhanced KA-induced Ca(2+) influx, while chronic Aβ (24 h) 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 1 mGluRs. We found that Aβ did not activate group 1 mGluRs 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

  13. Amyloid and tau cerebrospinal fluid biomarkers in HIV infection

    PubMed Central

    2009-01-01

    Background Because of the emerging intersections of HIV infection and Alzheimer's disease, we examined cerebrospinal fluid (CSF) biomarkers related of amyloid and tau metabolism in HIV-infected patients. Methods In this cross-sectional study we measured soluble amyloid precursor proteins alpha and beta (sAPPα and sAPPβ), amyloid beta fragment 1-42 (Aβ1-42), and total and hyperphosphorylated tau (t-tau and p-tau) in CSF of 86 HIV-infected (HIV+) subjects, including 21 with AIDS dementia complex (ADC), 25 with central nervous system (CNS) opportunistic infections and 40 without neurological symptoms and signs. We also measured these CSF biomarkers in 64 uninfected (HIV-) subjects, including 21 with Alzheimer's disease, and both younger and older controls without neurological disease. Results CSF sAPPα and sAPPβ concentrations were highly correlated and reduced in patients with ADC and opportunistic infections compared to the other groups. The opportunistic infection group but not the ADC patients had lower CSF Aβ1-42 in comparison to the other HIV+ subjects. CSF t-tau levels were high in some ADC patients, but did not differ significantly from the HIV+ neuroasymptomatic group, while CSF p-tau was not increased in any of the HIV+ groups. Together, CSF amyloid and tau markers segregated the ADC patients from both HIV+ and HIV- neuroasymptomatics and from Alzheimer's disease patients, but not from those with opportunistic infections. Conclusions Parallel reductions of CSF sAPPα and sAPPβ in ADC and CNS opportunistic infections suggest an effect of CNS immune activation or inflammation on neuronal amyloid synthesis or processing. Elevation of CSF t-tau in some ADC and CNS infection patients without concomitant increase in p-tau indicates neural injury without preferential accumulation of hyperphosphorylated tau as found in Alzheimer's disease. These biomarker changes define pathogenetic pathways to brain injury in ADC that differ from those of Alzheimer's disease

  14. 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

  15. Effects of wild type tau and disease-linked tau mutations on microtubule organization and intracellular trafficking.

    PubMed

    Yu, Dezhi; Feinstein, Stuart C; Valentine, Megan T

    2016-05-24

    We investigate the effects of transient expression of wild type (WT) and disease-linked mutations of tau (R406W, P301L, ΔN296) on cytoskeletal organization and cargo transport in COS-7 cells, which are natively tau-free. The introduction of tau proteins (either WT or mutant forms) leads to a dramatic restructuring of the microtubule cytoskeleton, as observed using immunofluorescence microscopy. Yet, this microtubule bundling and aggregation has a modest effect on the speed and travel distance of motor-driven cargo transport, as measured by the motions of fluorescently-labeled lysosomes. This suggests that localized transport events are insensitive to the global structure of the microtubule cytoskeleton. Importantly, we also found no evidence that the disease-linked tau mutants were particularly toxic; in fact we found that expression of mutant and WT tau had similar effects on overall microtubule structure and transport phenotypes. PMID:26674472

  16. New production mechanism of neutral Higgs bosons with right scalar tau neutrino as the LSP

    NASA Astrophysics Data System (ADS)

    Chou, C.-L.; Lai, H.-L.; Yuan1, C.-P.

    2000-09-01

    Inspired by the neutrino oscillation data, we consider the lightest tau sneutrino ν~τ1 (which is mostly the right tau sneutrino) to be the lightest supersymmetric particle (LSP) in the framework of the minimal supersymmetric Standard Model. Both the standard and the non-standard trilinear scalar coupling terms are included for the right tau sneutrino interactions. The decay branching ratio of ν~τ2-- >ν~τ1+h0 can become so large that the production rate of the lightest neutral Higgs boson (h0) can be largely enhanced at electron or hadron colliders, either from the direct production of ν~τ2 or from the decay of charginos, neutralinos, sleptons, and the cascade decay of squarks and gluinos, etc. Furthermore, because of the small LSP annihilation rate, ν~τ1 can be a good candidate for cold dark matter.

  17. Overexpression of Wild-Type Murine Tau Results in Progressive Tauopathy and Neurodegeneration

    PubMed Central

    Adams, Stephanie J.; Crook, Richard J.P.; DeTure, Michael; Randle, Suzanne J.; Innes, Amy E.; Yu, Xin Z.; Lin, Wen-Lang; Dugger, Brittany N.; McBride, Melinda; Hutton, Mike; Dickson, Dennis W.; McGowan, Eileen

    2009-01-01

    Here, we describe the generation and characterization of a novel tau transgenic mouse model (mTau) that overexpresses wild-type murine tau protein by twofold compared with endogenous levels. Transgenic tau expression was driven by a BAC transgene containing the entire wild-type mouse tau locus, including the endogenous promoter and the regulatory elements associated with the tau gene. The mTau model therefore differs from other tau models in that regulation of the genomic mouse transgene mimics that of the endogenous gene, including normal exon splicing regulation. Biochemical data from the mTau mice demonstrated that modest elevation of mouse tau leads to tau hyperphosphorylation at multiple pathologically relevant epitopes and accumulation of sarkosyl-insoluble tau. The mTau mice show a progressive increase in hyperphosphorylated tau pathology with age up to 15 to 18 months, which is accompanied by gliosis and vacuolization. In contrast, older mice show a decrease in tau pathology levels, which may represent hippocampal neuronal loss occurring in this wild-type model. Collectively, these results describe a novel model of tauopathy that develops pathological changes reminiscent of early stage Alzheimer’s disease and other related neurodegenerative diseases, achieved without overexpression of a mutant human tau transgene. This model will provide an important tool for understanding the early events leading to the development of tau pathology and a model for analysis of potential therapeutic targets for sporadic tauopathies. PMID:19717642

  18. The Dynamics and Turnover of Tau Aggregates in Cultured Cells: INSIGHTS INTO THERAPIES FOR TAUOPATHIES.

    PubMed

    Guo, Jing L; Buist, Arjan; Soares, Alberto; Callaerts, Kathleen; Calafate, Sara; Stevenaert, Frederik; Daniels, Joshua P; Zoll, Bryan E; Crowe, Alex; Brunden, Kurt R; Moechars, Diederik; Lee, Virginia M Y

    2016-06-17

    Filamentous tau aggregates, the hallmark lesions of Alzheimer disease (AD), play key roles in neurodegeneration. Activation of protein degradation systems has been proposed to be a potential strategy for removing pathological tau, but it remains unclear how effectively tau aggregates can be degraded by these systems. By applying our previously established cellular model system of AD-like tau aggregate induction using preformed tau fibrils, we demonstrate that tau aggregates induced in cells with regulated expression of full-length mutant tau can be gradually cleared when soluble tau expression is suppressed. This clearance is at least partially mediated by the autophagy-lysosome pathway, although both the ubiquitin-proteasome system and the autophagy-lysosome pathway are deficient in handling large tau aggregates. Importantly, residual tau aggregates left after the clearance phase leads to a rapid reinstatement of robust tau pathology once soluble tau expression is turned on again. Moreover, we succeeded in generating monoclonal cells persistently carrying tau aggregates without obvious cytotoxicity. Live imaging of GFP-tagged tau aggregates showed that tau inclusions are dynamic structures constantly undergoing "fission" and "fusion," which facilitate stable propagation of tau pathology in dividing cells. These findings provide a greater understanding of cell-to-cell transmission of tau aggregates in dividing cells and possibly neurons. PMID:27129267

  19. 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 (25 mg/kg) or saline (0.9%) from 5 to 7 months 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

  20. 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/).

  1. 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-τ. 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-τ performs favorably for stiff systems and that the LCLA-τ is also able to capture bimodal distributions unlike the CLA itself. The proposed LCLA-τ 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.

  2. Tau leaping of stiff stochastic chemical systems via local central limit approximation

    NASA Astrophysics Data System (ADS)

    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 S1↔S2. The proposed method uses a central limit approximation (CLA) locally over the tau leaping interval and is referred to as the LCLA-τ. 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-τ performs favorably for stiff systems and that the LCLA-τ is also able to capture bimodal distributions unlike the CLA itself. The proposed LCLA-τ 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.

  3. 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.

  4. LRRK2 Promotes Tau Accumulation, Aggregation and Release.

    PubMed

    Guerreiro, Patrícia Silva; Gerhardt, Ellen; Lopes da Fonseca, Tomás; Bähr, Mathias; Outeiro, Tiago Fleming; Eckermann, Katrin

    2016-07-01

    Mutations in the leucine-rich repeat kinase 2 (LRRK2) gene are known as the most frequent cause of familial Parkinson's disease (PD), but are also present in sporadic cases. The G2019S-LRRK2 mutation is located in the kinase domain of the protein, and has consistently been reported to promote a gain of kinase function. Several proteins have been reported as LRRK2 substrates and/or interactors, suggesting possible pathways involved in neurodegeneration in PD. Hyperphosphorylated Tau protein accumulates in neurofibrillary tangles, a typical pathological hallmark in Alzheimer's disease and frontotemporal dementia. In addition, it is also frequently found in the brains of PD patients. Although LRRK2 is a kinase, it appears that a putative interaction with Tau is phosphorylation-independent. However, the underlying mechanisms and the cellular consequences of this interaction are still unclear. In this study, we demonstrate an interaction between LRRK2 and Tau and that LRRK2 promotes the accumulation of non-monomeric and high-molecular weight (HMW) Tau species independent of its kinase activity. Interestingly, we found that LRRK2 increases Tau secretion, possibly as a consequence of an impairment of Tau proteasomal degradation. Our data highlight a mechanism through which LRRK2 regulates intracellular Tau levels, contributing to the progression of the pathology caused by the LRRK2-mediated proteasome impairment. In total, our findings suggest that the interplay between LRRK2 and proteasome activity might constitute a valid target for therapeutic intervention in PD. PMID:26014385

  5. Early Axonopathy Preceding Neurofibrillary Tangles in Mutant Tau Transgenic Mice

    PubMed Central

    Leroy, Karelle; Bretteville, Alexis; Schindowski, Katharina; Gilissen, Emmanuel; Authelet, Michèle; De Decker, Robert; Yilmaz, Zehra; Buée, Luc; Brion, Jean-Pierre

    2007-01-01

    Neurodegenerative diseases characterized by brain and spinal cord involvement often show widespread accumulations of tau aggregates. We have generated a transgenic mouse line (Tg30tau) expressing in the forebrain and the spinal cord a human tau protein bearing two pathogenic mutations (P301S and G272V). These mice developed age-dependent brain and hippocampal atrophy, central and peripheral axonopathy, progressive motor impairment with neurogenic muscle atrophy, and neurofibrillary tangles and had decreased survival. Axonal spheroids and axonal atrophy developed early before neurofibrillary tangles. Neurofibrillary inclusions developed in neurons at 3 months and were of two types, suggestive of a selective vulnerability of neurons to form different types of fibrillary aggregates. A first type of tau-positive neurofibrillary tangles, more abundant in the forebrain, were composed of ribbon-like 19-nm-wide filaments and twisted paired helical filaments. A second type of tau and neurofilament-positive neurofibrillary tangles, more abundant in the spinal cord and the brainstem, were composed of 10-nm-wide neurofilaments and straight 19-nm filaments. Unbiased stereological analysis indicated that total number of pyramidal neurons and density of neurons in the lumbar spinal cord were not reduced up to 12 months in Tg30tau mice. This Tg30tau model thus provides evidence that axonopathy precedes tangle formation and that both lesions can be dissociated from overt neuronal loss in selected brain areas but not from neuronal dysfunction. PMID:17690183

  6. Effects of macromolecular crowding and osmolyte on human Tau fibrillation.

    PubMed

    Wu, Yingying; Teng, Ningning; Li, Sen

    2016-09-01

    Tau fibrillation is reported to be involved in neurodegenerative disorders, such as Alzheimer's disease, in which the natural environment is very crowded in the cells. Understanding the role of crowding environments in regulating Tau fibrillation is of great importance for elucidating the etiology of these diseases. In this experiment, the effects of macromolecular crowding and osmolyte reagents in the crowding environment on Tau fibrillation were studied by thioflavin T binding, SDS-PAGE and TEM assays. Ficoll 70 and Dextran 70 of different concentrations were used as macromolecular crowding reagents inside the cells and showed a strong enhancing effect on the fibrillation of normal and hyperphosphorylated Tau. The enhancing effect of Dextran is stronger than that of Ficoll 70 at the same concentration. In addition, the cellular osmolyte sucrose was found to protect Tau against fibrillation, and inhibit the enhancing effect of macromolecular crowding on Tau fibrillation. A possible model for the fibrillation process of Tau and the effect of macromolecular crowding and osmolyte on this process was proposed based on these experimental results. The information obtained from our study can enhance the understanding of how proteins aggregate and avoid aggregation in crowded physiological environments and might lead to a better understanding of the molecular mechanisms of Alzheimer's disease in vivo. PMID:26683879

  7. Study of t anti-t production in tau jets channel at CDFII using neural networks

    SciTech Connect

    Amerio, Silvia; /Trento U.

    2005-12-01

    CDF (Collider Detector at Fermilab) is a particle detector located at Fermi National Laboratories, near Chicago. it allows to study decay products of p{bar p} collisions at center-of-mass energy of 1.96 TeV. During its first period of data taking (RunI), CDF observed for the first time the top quark (1995). The current period of data taking (RunII) is devoted to precise measurements of top properties and to search for new physics. This thesis work is about the top decay channel named {tau} + jets. A t{bar t} pair decays in two W bosons and two b quarks. In a {tau} + jets event, one out of the two W decays into two jets of hadrons, while the other produces a {tau} lepton and a neutrino; the {tau} decays semileptonically in one or more charged and neutral pions while b quarks hadronize producing two jets of particles. Thus the final state of a {tau} + jets event has this specific signature: five jets, one {tau}-like, i.e. narrow and with low track multiplicity, two from b quarks, two from a W boson and a large amount of missing energy from two {tau} neutrinos. They search for this signal in 311 pb{sup -1} of data collected with TOP{_}MULTIJET trigger. They use neural networks to separate signal from background and on the selected sample they perform a t{bar t} production cross section measurement. The thesis is structured as follows: in Chapter 1 they outline the physics of top and {tau}, concentrating on their discovery, production mechanisms and current physics results involving them. Chapter 2 is devoted to the description of the experimental setup: the accelerator complex first and CDF detector then. The trigger system is described in Chapter 3, while Chapter 4 shows how particles are reconstructed exploiting information from different CDF subdetectors. With Chapter 5 they begin to present their analysis: we use a feed forward neural network based on a minimization algorithm developed in Trento University, called Reactive Taboo Search (RTS), especially designed

  8. Aging-related tau astrogliopathy (ARTAG): harmonized evaluation strategy.

    PubMed

    Kovacs, Gabor G; Ferrer, Isidro; Grinberg, Lea T; Alafuzoff, Irina; Attems, Johannes; Budka, Herbert; Cairns, Nigel J; Crary, John F; Duyckaerts, Charles; Ghetti, Bernardino; Halliday, Glenda M; Ironside, James W; Love, Seth; Mackenzie, Ian R; Munoz, David G; Murray, Melissa E; Nelson, Peter T; Takahashi, Hitoshi; Trojanowski, John Q; Ansorge, Olaf; Arzberger, Thomas; Baborie, Atik; Beach, Thomas G; Bieniek, Kevin F; Bigio, Eileen H; Bodi, Istvan; Dugger, Brittany N; Feany, Mel; Gelpi, Ellen; Gentleman, Stephen M; Giaccone, Giorgio; Hatanpaa, Kimmo J; Heale, Richard; Hof, Patrick R; Hofer, Monika; Hortobágyi, Tibor; Jellinger, Kurt; Jicha, Gregory A; Ince, Paul; Kofler, Julia; Kövari, Enikö; Kril, Jillian J; Mann, David M; Matej, Radoslav; McKee, Ann C; McLean, Catriona; Milenkovic, Ivan; Montine, Thomas J; Murayama, Shigeo; Lee, Edward B; Rahimi, Jasmin; Rodriguez, Roberta D; Rozemüller, Annemieke; Schneider, Julie A; Schultz, Christian; Seeley, William; Seilhean, Danielle; Smith, Colin; Tagliavini, Fabrizio; Takao, Masaki; Thal, Dietmar Rudolf; Toledo, Jon B; Tolnay, Markus; Troncoso, Juan C; Vinters, Harry V; Weis, Serge; Wharton, Stephen B; White, Charles L; Wisniewski, Thomas; Woulfe, John M; Yamada, Masahito; Dickson, Dennis W

    2016-01-01

    Pathological accumulation of abnormally phosphorylated tau protein in astrocytes is a frequent, but poorly characterized feature of the aging brain. Its etiology is uncertain, but its presence is sufficiently ubiquitous to merit further characterization and classification, which may stimulate clinicopathological studies and research into its pathobiology. This paper aims to harmonize evaluation and nomenclature of aging-related tau astrogliopathy (ARTAG), a term that refers to a morphological spectrum of astroglial pathology detected by tau immunohistochemistry, especially with phosphorylation-dependent and 4R isoform-specific antibodies. ARTAG occurs mainly, but not exclusively, in individuals over 60 years of age. Tau-immunoreactive astrocytes in ARTAG include thorn-shaped astrocytes at the glia limitans and in white matter, as well as solitary or clustered astrocytes with perinuclear cytoplasmic tau immunoreactivity that extends into the astroglial processes as fine fibrillar or granular immunopositivity, typically in gray matter. Various forms of ARTAG may coexist in the same brain and might reflect different pathogenic processes. Based on morphology and anatomical distribution, ARTAG can be distinguished from primary tauopathies, but may be concurrent with primary tauopathies or other disorders. We recommend four steps for evaluation of ARTAG: (1) identification of five types based on the location of either morphologies of tau astrogliopathy: subpial, subependymal, perivascular, white matter, gray matter; (2) documentation of the regional involvement: medial temporal lobe, lobar (frontal, parietal, occipital, lateral temporal), subcortical, brainstem; (3) documentation of the severity of tau astrogliopathy; and (4) description of subregional involvement. Some types of ARTAG may underlie neurological symptoms; however, the clinical significance of ARTAG is currently uncertain and awaits further studies. The goal of this proposal is to raise awareness of

  9. Short Fibrils Constitute the Major Species of Seed-Competent Tau in the Brains of Mice Transgenic for Human P301S Tau

    PubMed Central

    Jackson, Samuel J.; Kerridge, Caroline; Cooper, Jane; Cavallini, Annalisa; Falcon, Benjamin; Cella, Claire V.; Landi, Alessia; Szekeres, Philip G.; Murray, Tracey K.; Ahmed, Zeshan; Goedert, Michel; Hutton, Michael; O'Neill, Michael J.

    2016-01-01

    The interneuronal propagation of aggregated tau is believed to play an important role in the pathogenesis of human tauopathies. It requires the uptake of seed-competent tau into cells, seeding of soluble tau in recipient neurons and release of seeded tau into the extracellular space to complete the cycle. At present, it is not known which tau species are seed-competent. Here, we have dissected the molecular characteristics of seed-competent tau species from the TgP301S tau mouse model using various biochemical techniques and assessed their seeding ability in cell and animal models. We found that sucrose gradient fractions from brain lysates seeded cellular tau aggregation only when large (>10 mer) aggregated, hyperphosphorylated (AT8- and AT100-positive) and nitrated tau was present. In contrast, there was no detectable seeding by fractions containing small, oligomeric (<6 mer) tau. Immunodepletion of the large aggregated AT8-positive tau strongly reduced seeding; moreover, fractions containing these species initiated the formation and spreading of filamentous tau pathology in vivo, whereas fractions containing tau monomers and small oligomeric assemblies did not. By electron microscopy, seed-competent sucrose gradient fractions contained aggregated tau species ranging from ring-like structures to small filaments. Together, these findings indicate that a range of filamentous tau aggregates are the major species that underlie the spreading of tau pathology in the P301S transgenic model. SIGNIFICANCE STATEMENT The spread of tau pathology from neuron to neuron is postulated to account for, or at least to contribute to, the overall propagation of tau pathology during the development of human tauopathies including Alzheimer's disease. It is therefore important to characterize the native tau species responsible for this process of seeding and pathology spreading. Here, we use several biochemical techniques to dissect the molecular characteristics of native tau protein

  10. Short Fibrils Constitute the Major Species of Seed-Competent Tau in the Brains of Mice Transgenic for Human P301S Tau.

    PubMed

    Jackson, Samuel J; Kerridge, Caroline; Cooper, Jane; Cavallini, Annalisa; Falcon, Benjamin; Cella, Claire V; Landi, Alessia; Szekeres, Philip G; Murray, Tracey K; Ahmed, Zeshan; Goedert, Michel; Hutton, Michael; O'Neill, Michael J; Bose, Suchira

    2016-01-20

    The interneuronal propagation of aggregated tau is believed to play an important role in the pathogenesis of human tauopathies. It requires the uptake of seed-competent tau into cells, seeding of soluble tau in recipient neurons and release of seeded tau into the extracellular space to complete the cycle. At present, it is not known which tau species are seed-competent. Here, we have dissected the molecular characteristics of seed-competent tau species from the TgP301S tau mouse model using various biochemical techniques and assessed their seeding ability in cell and animal models. We found that sucrose gradient fractions from brain lysates seeded cellular tau aggregation only when large (>10 mer) aggregated, hyperphosphorylated (AT8- and AT100-positive) and nitrated tau was present. In contrast, there was no detectable seeding by fractions containing small, oligomeric (<6 mer) tau. Immunodepletion of the large aggregated AT8-positive tau strongly reduced seeding; moreover, fractions containing these species initiated the formation and spreading of filamentous tau pathology in vivo, whereas fractions containing tau monomers and small oligomeric assemblies did not. By electron microscopy, seed-competent sucrose gradient fractions contained aggregated tau species ranging from ring-like structures to small filaments. Together, these findings indicate that a range of filamentous tau aggregates are the major species that underlie the spreading of tau pathology in the P301S transgenic model. Significance statement: The spread of tau pathology from neuron to neuron is postulated to account for, or at least to contribute to, the overall propagation of tau pathology during the development of human tauopathies including Alzheimer's disease. It is therefore important to characterize the native tau species responsible for this process of seeding and pathology spreading. Here, we use several biochemical techniques to dissect the molecular characteristics of native tau protein

  11. Tau function of the CKP hierarchy and nonlinearizable virasoro symmetries

    NASA Astrophysics Data System (ADS)

    Chang, Liang; Wu, Chao-Zhong

    2013-09-01

    We introduce a single tau function that represents the C-type Kadomtsev-Petviashvili (CKP) hierarchy in a generalized Hirota ‘bilinear’ equation. The actions on the tau function by additional symmetries for the hierarchy are also calculated, which involve strictly more than a central extension of the w^C_\\infty -algebra. As an application, for Drinfeld-Sokolov hierarchies associated to affine Kac-Moody algebras of type C, we obtain a formula to compute the obstacles in linearizing their Virasoro symmetries and hence prove the Virasoro symmetries to be nonlinearizable when acting on the tau function.

  12. Electroweak and Higgs Measurements Using Tau Final States with the LHCb Detector

    NASA Astrophysics Data System (ADS)

    Ilten, Philip

    Spin correlations for tau lepton decays are included in the Pythia 8 event generation software with a framework which can be expanded to include the decays of particles other than the tau lepton. The spin correlations for the decays of tau leptons produced from electroweak and Higgs bosons are calculated. Decays of the tau lepton using sophisticated resonance models are included in Pythia 8 for all channels with experimentally observed branching fractions greater than 0.04%. The mass distributions for the decay products of these channels calculated with Pythia 8 are validated against the equivalent distributions from the Herwig++ and Tauola event generators. The technical implementation of the tau lepton spin correlations and decays in Pythia 8 is described. A measurement of the inclusive Z to di-tau cross-section using 1.0 inverse fb of data from pp collisions at sqrt(s) = 7 TeV collected with the LHCb detector is presented. Reconstructed final states containing two muons, a muon and an electron, a muon and a charged hadron, or an electron and a charged hadron are selected as Z to di-tau candidates. The cross-section for Z bosons with a mass between 60 and 120 GeV decaying into tau leptons with pseudo-rapidities between 2.0 and 4.5 and transverse momenta greater than 20 GeV is measured to be 72.3 +/- 3.5 +/- 2.9 +/- 2.5 pb. The first uncertainty is statistical, the second uncertainty is systematic, and the third is to due the integrated luminosity uncertainty. The Z to di-tau to Z to di-muon cross-section ratio is found to be 0.94 +/- 0.09 and the Z to di-tau to Z to di-electron cross-section ratio is found to be 0.95 +/- 0.07. The uncertainty on these ratios is the combined statistical, systematic, and luminosity uncertainties. Limits on the production of neutral Higgs bosons decaying into tau lepton pairs with pseudo-rapidities between 2.0 and 4.5 are set at a 95% confidence level using the same LHCb dataset. A model independent upper limit on the production of

  13. Conformation determines the seeding potencies of native and recombinant Tau aggregates.

    PubMed

    Falcon, Benjamin; Cavallini, Annalisa; Angers, Rachel; Glover, Sarah; Murray, Tracey K; Barnham, Luanda; Jackson, Samuel; O'Neill, Michael J; Isaacs, Adrian M; Hutton, Michael L; Szekeres, Philip G; Goedert, Michel; Bose, Suchira

    2015-01-01

    Intracellular Tau inclusions are a pathological hallmark of several neurodegenerative diseases, collectively known as the tauopathies. They include Alzheimer disease, tangle-only dementia, Pick disease, argyrophilic grain disease, chronic traumatic encephalopathy, progressive supranuclear palsy, and corticobasal degeneration. Tau pathology appears to spread through intercellular propagation, requiring the formation of assembled "prion-like" species. Several cell and animal models have been described that recapitulate aspects of this phenomenon. However, the molecular characteristics of seed-competent Tau remain unclear. Here, we have used a cell model to understand the relationships between Tau structure/phosphorylation and seeding by aggregated Tau species from the brains of mice transgenic for human mutant P301S Tau and full-length aggregated recombinant P301S Tau. Deletion of motifs (275)VQIINK(280) and (306)VQIVYK(311) abolished the seeding activity of recombinant full-length Tau, suggesting that its aggregation was necessary for seeding. We describe conformational differences between native and synthetic Tau aggregates that may account for the higher seeding activity of native assembled Tau. When added to aggregated Tau seeds from the brains of mice transgenic for P301S Tau, soluble recombinant Tau aggregated and acquired the molecular properties of aggregated Tau from transgenic mouse brain. We show that seeding is conferred by aggregated Tau that enters cells through macropinocytosis and seeds the assembly of endogenous Tau into filaments. PMID:25406315

  14. Loss of medial septum cholinergic neurons in THY-Tau22 mouse model: what links with tau pathology?

    PubMed

    Belarbi, K; Burnouf, S; Fernandez-Gomez, F-J; Desmercières, J; Troquier, L; Brouillette, J; Tsambou, L; Grosjean, M-E; Caillierez, R; Demeyer, D; Hamdane, M; Schindowski, K; Blum, D; Buée, L

    2011-09-01

    Alzheimer's disease (AD) is a neurodegenerative disorder histologically defined by the cerebral accumulation of amyloid deposits and neurofibrillary tangles composed of hyperphosphorylated tau proteins. Loss of basal forebrain cholinergic neurons is another hallmark of the disease thought to contribute to the cognitive dysfunctions. To this date, the mechanisms underlying cholinergic neurons degeneration remain uncertain. The present study aimed to investigate the relationship between neurofibrillary degeneration and cholinergic defects in AD using THY-Tau22 transgenic mouse model exhibiting a major hippocampal AD-like tau pathology and hyperphosphorylated tau species in the septohippocampal pathway. Here, we report that at a time THY-Tau22 mice display strong reference memory alterations, the retrograde transport of fluorogold through the septohippocampal pathway is altered. This impairment is associated with a significant reduction in the number of choline acetyltransferase (ChAT)-immunopositive cholinergic neurons in the medial septum. Analysis of nerve growth factor (NGF) levels supports an accumulation of the mature neurotrophin in the hippocampus of THY-Tau22 mice, consistent with a decrease of its uptake or retrograde transport by cholinergic terminals. Finally, our data strongly support that tau pathology could be instrumental in the cholinergic neuronal loss observed in AD. PMID:21605043

  15. Pattern of tau hyperphosphorylation and neurotransmitter markers in the brainstem of senescent tau filament forming transgenic mice.

    PubMed

    Morcinek, Kerstin; Köhler, Christoph; Götz, Jürgen; Schröder, Hannsjörg

    2013-02-25

    The early occurrence of brainstem-related symptoms, e.g. gait and balance impairment, apathy and depression in Alzheimer's disease patients suggests brainstem involvement in the initial pathogenesis. To address the question whether tau filament forming mice expressing mutated human tau mirror histopathological changes observed in Alzheimer brainstem, the degree and distribution of neurofibrillary lesions as well as the pattern of cholinergic and monoaminergic neurons were investigated. The expression of the human tau transgene was observed in multiple brainstem nuclei, particularly in the magnocellular reticular formation, vestibular nuclei, cranial nerve motor nuclei, sensory trigeminal nerve nuclei, inferior and superior colliculi, periaqueductal and pontine gray matter, and the red nucleus. Most of the human tau-immunoreactive cell groups also showed tau hyperphosphorylation at the epitopes Thr231/Ser235 and Ser202/Thr205, while abnormal tau phosphorylation at the epitope Ser422 or silver stained structures were almost totally lacking. We found no obvious differences in distribution and density of cholinergic and monoaminergic neurons between tau-transgenic and wild type mice. Although numerous brainstem nuclei in our model expressed human tau protein, the development of neurofibrillary tangles, neuropil threads and ghost tangles was rare and likewise its distribution differed largely from Alzheimer's disease pattern. The number of monoaminergic neurons remained unchanged in the transgenic mice, while monoaminergic nuclei in Alzheimer brainstem showed a distinct neuronal loss. However, the distribution of pretangle-affected neurons in the tau-transgenic mice partly resembled those seen in progressive supranuclear palsy, presenting these animals as a model to examine brainstem pathogenesis of progressive supranuclear palsy. PMID:23261664

  16. The neuritic plaque facilitates pathological conversion of tau in an Alzheimer's disease mouse model

    PubMed Central

    Li, Tong; Braunstein, Kerstin E.; Zhang, Juhong; Lau, Ashley; Sibener, Leslie; Deeble, Christopher; Wong, Philip C.

    2016-01-01

    A central question in Alzheimer's Disease (AD) is whether the neuritic plaque is necessary and sufficient for the development of tau pathology. Hyperphosphorylation of tau is found within dystrophic neurites surrounding β-amyloid deposits in AD mouse models but the pathological conversion of tau is absent. Likewise, expression of a human tau repeat domain in mice is insufficient to drive the pathological conversion of tau. Here we developed an Aβ-amyloidosis mouse model that expresses the human tau repeat domain and show that in these mice, the neuritic plaque facilitates the pathological conversion of wild-type tau. We show that this tau fragment seeds the neuritic plaque-dependent pathological conversion of wild-type tau that spreads from the cortex and hippocampus to the brain stem. These results establish that in addition to the neuritic plaque, a second determinant is required to drive the conversion of wild-type tau. PMID:27373369

  17. Measurements of the Top-quark Mass and the $t\\bar{t}$ Cross Section in the Hadronic $\\tau +$ Jets Decay Channel 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.; Arisawa, T.; Artikov, A.; /Dubna, JINR /Texas A-M

    2012-08-01

    We present the first direct measurement of the top-quark mass using t{bar t} events decaying in the hadronic {tau} + jets decay channel. Using data corresponding to an integrated luminosity of 2.2 fb{sup -1} collected by the CDF II detector in p{bar p} collisions at {radical}s = 1.96 TeV at the Fermilab Tevatron, we measure the t{bar t} cross section, {sigma}{sub t{bar t}}, and the top-quark mass, M{sub top}. We extract M{sub top} from a likelihood based on per-event probabilities calculated with leading-order signal and background matrix elements. We measure {sigma}{sub t{bar t}} = 8.8 {+-} 3.3 (stat) {+-} 2.2 (syst) pb and M{sub top} = 172.7 {+-} 9.3 (stat) {+-} 3.7 (syst) GeV/c{sup 2}.

  18. Planet Formation in the GG Tau A System?

    NASA Astrophysics Data System (ADS)

    Dutrey, A.

    2015-12-01

    Located at 140 pc, the environment of the young hierarchical TTauri star system GG Tau A remains a unique laboratory to study tidal interactions and planet formation. We report new ALMA observations of the triple star GG Tau A performed at 0.5mm and in CO J=6-5 at resolution of 0.3 arcsecond. These new images resolve out the massive and narrow dust ring and reveal that a large amount of CO gas is streaming inside the cavity or the gravitationally unstable area. The dust and gas disk surrounding GG Tau Aa which is separated by 35 AU from the binary GG Tau Ab, would not survive without regular replenishment form these streamers.

  19. Tau/Amyloid Beta 42 Peptide Test (Alzheimer Biomarkers)

    MedlinePlus

    ... page: Was this page helpful? Also known as: Alzheimer Biomarkers Formal name: Tau Protein and Amyloid Beta ... supplemental tests to help establish a diagnosis of Alzheimer disease and to distinguish between AD and other ...

  20. Measurement of \\mathcal{B}(\\tau^{-}\\-->\\bar{K^{0}}\\pi^{-}\

    SciTech Connect

    Wren, A

    2008-08-13

    A preliminary measurement of the branching fraction {Beta}({tau}{sup -} {yields} K{sub S}{sup 0}{pi}{sup -}{nu}{sub {tau}}) is made using 384.6 fb{sup -1} of e{sup +}e{sup -} collision data provided by the PEP-II collider, operating primarily at {radical}s = 10.58 GeV, and recorded using the BABAR detector. From this they measure: {Beta}({tau}{sup -} {yields} {bar K}{sup 0}{pi}{sup -}{nu}{sub {tau}}) = (0.840 {+-} 0.004(stat) {+-} 0.023(syst))%. This result is the most precise measurement to date and is consistent with the world average.

  1. Argonne Tau-charm factory collider design study

    SciTech Connect

    Teng, L.C.; Crosbie, E.A.; Norem, J.

    1995-12-01

    The design approach and design principles for a Tau-charm Factory at Argonne were studied. These studies led to a set of preliminary parameters and tentative component features as presented in this paper.

  2. Measurements of the Top Anti-Top Production Cross Section and Top Quark Mass in the Hadronically Decaying Tau + Jets Decay Channel at CDF

    SciTech Connect

    Hare, Daryl Curtis

    2011-01-01

    In this thesis, we present the first exclusive observation of the t-t → hadronic τ + jets decay channel. Using these events, we measure the t-t pair production cross section and the top quark mass in 2.2 fb-1 of data collected with the Collider Detector at Fermilab (CDF). The Tevatron accelerator at Fermilab provides collisions of protons and anti-protons at a center-of-mass energy of √s = 1.96 TeV and is one of only two accelerators in the world with enough energy to produce top quarks. With a branching fraction of nearly 10%, the hadronic τ + jets decay channel is the third largest t-t decay mode, and it has only been minimally explored. This the first measurement of the t-t pair production cross section in this decay channel at CDF and the first measurement of the top quark mass in this decay channel in the world. The analysis introduces a new method to recover the total momentum of the ν produced in the τ decay and an artificial neural network to reduce the contribution from the largest background source, QCD multijet background. The t-t pair production cross section is extracted by minimizing a negative log likelihood function which compares the number of observed events to the number of expected events for a given t-t cross section. The top quark mass is extracted by minimizing a negative log likelihood function built from signal and ii background probabilities which are based on the matrix elements for t-t production and decay and W + 4 parton production, respectively. Using events selected with exactly 1 hadronically decaying τ, exactly 4 jets with at least 1 identified as having originated from a b quark, and large missing transverse energy, we measure the t-t pair production cross section to be 8.8 ± 3.3 (stat.) ± 2.2 (syst.) pb and the top quark mass to be 172.7±9.3 (stat.) ±3.7 (syst.) GeV. We find both values to be in good agreement with

  3. Physiological and pathological phosphorylation of tau by Cdk5.

    PubMed

    Kimura, Taeko; Ishiguro, Koichi; Hisanaga, Shin-Ichi

    2014-01-01

    Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer's disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). Mutations in the tau gene MAPT are a cause of FTDP-17, and the mutated tau proteins are hyperphosphorylated in patient brains. Thus, it is important to determine the molecular mechanism of hyperphosphorylation of tau to understand the pathology of these diseases collectively called tauopathy. Tau is phosphorylated at many sites via several protein kinases, and a characteristic is phosphorylation at Ser/Thr residues in Ser/Thr-Pro sequences, which are targeted by proline-directed protein kinases such as ERK, GSK3β, and Cdk5. Among these kinases, Cdk5 is particularly interesting because it could be abnormally activated in AD. Cdk5 is a member of the cyclin-dependent kinases (Cdks), but in contrast to the major Cdks, which promote cell cycle progression in proliferating cells, Cdk5 is activated in post-mitotic neurons via the neuron-specific activator p35. Cdk5-p35 plays a critical role in brain development and physiological synaptic activity. In contrast, in disease brains, Cdk5 is thought to be hyperactivated by p25, which is the N-terminal truncated form of p35 and is generated by cleavage with calpain. Several reports have indicated that tau is hyperphosphorylated by Cdk5-p25. However, normal and abnormal phosphorylation of tau by Cdk5 is still not completely understood. In this article, we summarize the physiological and pathological phosphorylation of tau via Cdk5. PMID:25076872

  4. Physics of a high-luminosity Tau-Charm Factory

    SciTech Connect

    King, M.E.

    1992-10-01

    This paper highlights the physics capabilities of a Tau-Charm Factory; i.e., high luminosity ({approximately}10{sup 33}cm{sup {minus}2}s{sup {minus}1}) e{sup +}e{sup {minus}} collider operating in the center-of-mass energy range of 3-5 GeV, with a high-precision, general-purpose detector. Recent developments in {tau} and charm physics are emphasized.

  5. Physiological and pathological phosphorylation of tau by Cdk5

    PubMed Central

    Kimura, Taeko; Ishiguro, Koichi; Hisanaga, Shin-ichi

    2014-01-01

    Hyperphosphorylation of microtubule-associated protein tau is one of the major pathological events in Alzheimer’s disease (AD) and other related neurodegenerative diseases, including frontotemporal dementia with parkinsonism linked to chromosome 17 (FTDP-17). Mutations in the tau gene MAPT are a cause of FTDP-17, and the mutated tau proteins are hyperphosphorylated in patient brains. Thus, it is important to determine the molecular mechanism of hyperphosphorylation of tau to understand the pathology of these diseases collectively called tauopathy. Tau is phosphorylated at many sites via several protein kinases, and a characteristic is phosphorylation at Ser/Thr residues in Ser/Thr-Pro sequences, which are targeted by proline-directed protein kinases such as ERK, GSK3β, and Cdk5. Among these kinases, Cdk5 is particularly interesting because it could be abnormally activated in AD. Cdk5 is a member of the cyclin-dependent kinases (Cdks), but in contrast to the major Cdks, which promote cell cycle progression in proliferating cells, Cdk5 is activated in post-mitotic neurons via the neuron-specific activator p35. Cdk5-p35 plays a critical role in brain development and physiological synaptic activity. In contrast, in disease brains, Cdk5 is thought to be hyperactivated by p25, which is the N-terminal truncated form of p35 and is generated by cleavage with calpain. Several reports have indicated that tau is hyperphosphorylated by Cdk5-p25. However, normal and abnormal phosphorylation of tau by Cdk5 is still not completely understood. In this article, we summarize the physiological and pathological phosphorylation of tau via Cdk5. PMID:25076872

  6. Acetylation mimic of lysine 280 exacerbates human Tau neurotoxicity in vivo

    PubMed Central

    Gorsky, Marianna Karina; Burnouf, Sylvie; Dols, Jacqueline; Mandelkow, Eckhard; Partridge, Linda

    2016-01-01

    Dysfunction and accumulation of the microtubule-associated human Tau (hTau) protein into intraneuronal aggregates is observed in many neurodegenerative disorders including Alzheimer’s disease (AD). Reversible lysine acetylation has recently emerged as a post-translational modification that may play an important role in the modulation of hTau pathology. Acetylated hTau species have been observed within hTau aggregates in human AD brains and multi-acetylation of hTau in vitro regulates its propensity to aggregate. However, whether lysine acetylation at position 280 (K280) modulates hTau-induced toxicity in vivo is unknown. We generated new Drosophila transgenic models of hTau pathology to evaluate the contribution of K280 acetylation to hTau toxicity, by analysing the respective toxicity of pseudo-acetylated (K280Q) and pseudo-de-acetylated (K280R) mutant forms of hTau. We observed that mis-expression of pseudo-acetylated K280Q-hTau in the adult fly nervous system potently exacerbated fly locomotion defects and photoreceptor neurodegeneration. In addition, modulation of K280 influenced total hTau levels and phosphorylation without changing hTau solubility. Altogether, our results indicate that pseudo-acetylation of the single K280 residue is sufficient to exacerbate hTau neurotoxicity in vivo, suggesting that acetylated K280-hTau species contribute to the pathological events leading to neurodegeneration in AD. PMID:26940749

  7. SUMOylation at K340 inhibits tau degradation through deregulating its phosphorylation and ubiquitination.

    PubMed

    Luo, Hong-Bin; Xia, Yi-Yuan; Shu, Xi-Ji; Liu, Zan-Chao; Feng, Ye; Liu, Xing-Hua; Yu, Guang; Yin, Gang; Xiong, Yan-Si; Zeng, Kuan; Jiang, Jun; Ye, Keqiang; Wang, Xiao-Chuan; Wang, Jian-Zhi

    2014-11-18

    Intracellular accumulation of the abnormally modified tau is hallmark pathology of Alzheimer's disease (AD), but the mechanism leading to tau aggregation is not fully characterized. Here, we studied the effects of tau SUMOylation on its phosphorylation, ubiquitination, and degradation. We show that tau SUMOylation induces tau hyperphosphorylation at multiple AD-associated sites, whereas site-specific mutagenesis of tau at K340R (the SUMOylation site) or simultaneous inhibition of tau SUMOylation by ginkgolic acid abolishes the effect of small ubiquitin-like modifier protein 1 (SUMO-1). Conversely, tau hyperphosphorylation promotes its SUMOylation; the latter in turn inhibits tau degradation with reduction of solubility and ubiquitination of tau proteins. Furthermore, the enhanced SUMO-immunoreactivity, costained with the hyperphosphorylated tau, is detected in cerebral cortex of the AD brains, and β-amyloid exposure of rat primary hippocampal neurons induces a dose-dependent SUMOylation of the hyperphosphorylated tau. Our findings suggest that tau SUMOylation reciprocally stimulates its phosphorylation and inhibits the ubiquitination-mediated tau degradation, which provides a new insight into the AD-like tau accumulation. PMID:25378699

  8. Critical role of acetylation in tau-mediated neurodegeneration and cognitive deficits.

    PubMed

    Min, Sang-Won; Chen, Xu; Tracy, Tara E; Li, Yaqiao; Zhou, Yungui; Wang, Chao; Shirakawa, Kotaro; Minami, S Sakura; Defensor, Erwin; Mok, Sue Ann; Sohn, Peter Dongmin; Schilling, Birgit; Cong, Xin; Ellerby, Lisa; Gibson, Bradford W; Johnson, Jeffrey; Krogan, Nevan; Shamloo, Mehrdad; Gestwicki, Jason; Masliah, Eliezer; Verdin, Eric; Gan, Li

    2015-10-01

    Tauopathies, including frontotemporal dementia (FTD) and Alzheimer's disease (AD), are neurodegenerative diseases in which tau fibrils accumulate. Recent evidence supports soluble tau species as the major toxic species. How soluble tau accumulates and causes neurodegeneration remains unclear. Here we identify tau acetylation at Lys174 (K174) as an early change in AD brains and a critical determinant in tau homeostasis and toxicity in mice. The acetyl-mimicking mutant K174Q slows tau turnover and induces cognitive deficits in vivo. Acetyltransferase p300-induced tau acetylation is inhibited by salsalate and salicylate, which enhance tau turnover and reduce tau levels. In the PS19 transgenic mouse model of FTD, administration of salsalate after disease onset inhibited p300 activity, lowered levels of total tau and tau acetylated at K174, rescued tau-induced memory deficits and prevented hippocampal atrophy. The tau-lowering and protective effects of salsalate were diminished in neurons expressing K174Q tau. Targeting tau acetylation could be a new therapeutic strategy against human tauopathies. PMID:26390242

  9. Tau triage decisions mediated by the chaperone network.

    PubMed

    Cook, Casey; Petrucelli, Leonard

    2013-01-01

    The pathological accumulation of the microtubule-binding protein tau is linked to an increasing number of neurodegenerative conditions associated with aging, though the mechanisms by which tau accumulates in disease are unclear. In this review, we will summarize our previous research assessing the mechanism of action, as well as the therapeutic potential of Hsp90 inhibition for the treatment of tauopathies. Specifically, we describe the development of a high-throughput screening approach to identify and rank compounds, and demonstrate the selective elimination of aberrant p-tau species in the brain following treatment with an Hsp90 inhibitor. Additionally, we identify CHIP as an essential component of the Hsp90 chaperone complex that mediates tau degradation, and present evidence to suggest that CHIP functions to identify and sequester neurotoxic tau species. Finally, we discuss recent data identifying an additional mechanism by which CHIP modulates protein triage decisions involving Hsp90. Specifically, CHIP indirectly regulates Hsp90 chaperone activity by modulating steady-state levels of the Hsp90 deacetylase, HDAC6, thus influencing both the acetylation state and function of Hsp90. Thus future research directions will focus on the manipulation of this network to promote degradation of pathogenic tau species in disease. PMID:22596270

  10. The triple binary star EQ Tau with an active component

    SciTech Connect

    Li, K.; Hu, S.-M.; Qian, S.-B.; He, J.-J. E-mail: likai@ynao.ac.cn

    2014-05-01

    New photometric data of EQ Tau observed in 2010 and 2013 are presented. Light curves obtained in 2000 and 2004 by Yuan and Qian and 2001 by Yang and Liu, together with our two newly determined sets of light curves, were analyzed using the Wilson-Devinney code. The five sets of light curves exhibit very obvious variations, implying that the light curves of EQ Tau show a strong O'Connell effect. We found that EQ Tau is an A-type shallow contact binary with a contact degree of f = 11.8%; variable dark spots on the primary component of EQ Tau were also observed. Using 10 new times of minimum light, together with those collected from the literature, the orbital period change of EQ Tau was analyzed. We found that its orbital period includes a secular decrease (dP/dt = –3.63 × 10{sup –8} days yr{sup –1}) and a cyclic oscillation (A {sub 3} = 0.0058 days and P {sub 3} = 22.7 yr). The secular increase of the period can be explained by mass transfer from the more massive component to the less massive one or/and angular momentum loss due to a magnetic stellar wind. The Applegate mechanism cannot explain the cyclic orbital period change. A probable transit-like event was observed in 2010. Therefore, the cyclic orbital period change of EQ Tau may be due to the light time effect of a third body.

  11. Potent inhibition of tau fibrillization with a multivalent ligand

    SciTech Connect

    Honson, Nicolette S.; Jensen, Jordan R.; Darby, Michael V.; Kuret, Jeff

    2007-11-09

    Small-molecule inhibitors of tau fibrillization are under investigation as tools for interrogating the tau aggregation pathway and as potential therapeutic agents for Alzheimer's disease. Established inhibitors include thiacarbocyanine dyes, which can inhibit recombinant tau fibrillization in the presence of anionic surfactant aggregation inducers. In an effort to increase inhibitory potency, a cyclic bis-thiacarbocyanine molecule containing two thiacarbocyanine moieties was synthesized and characterized with respect to tau fibrillization inhibitory activity by electron microscopy and ligand aggregation state by absorbance spectroscopy. Results showed that the inhibitory activity of the bis-thiacarbocyanine was qualitatively similar to a monomeric cyanine dye, but was more potent with 50% inhibition achieved at {approx}80 nM concentration. At all concentrations tested in aqueous solution, the bis-thiacarbocyanine collapsed to form a closed clamshell structure. However, the presence of tau protein selectively stabilized the open conformation. These results suggest that the inhibitory activity of bis-thiacarbocyanine results from multivalency, and reveal a route to more potent tau aggregation inhibitors.

  12. Quantitative Analysis of Tau-Microtubule Interaction Using FRET

    PubMed Central

    Di Maïo, Isabelle L.; Barbier, Pascale; Allegro, Diane; Brault, Cédric; Peyrot, Vincent

    2014-01-01

    The interaction between the microtubule associated protein, tau and the microtubules is investigated. A fluorescence resonance energy transfer (FRET) assay was used to determine the distance separating tau to the microtubule wall, as well as the binding parameters of the interaction. By using microtubules stabilized with Flutax-2 as donor and tau labeled with rhodamine as acceptor, a donor-to-acceptor distance of 54 ± 1 Å was found. A molecular model is proposed in which Flutax-2 is directly accessible to tau-rhodamine molecules for energy transfer. By titration, we calculated the stoichiometric dissociation constant to be equal to 1.0 ± 0.5 µM. The influence of the C-terminal tails of αβ-tubulin on the tau-microtubule interaction is presented once a procedure to form homogeneous solution of cleaved tubulin has been determined. The results indicate that the C-terminal tails of α- and β-tubulin by electrostatic effects and of recruitment seem to be involved in the binding mechanism of tau. PMID:25196605

  13. Preliminary Measurement of B(tau- ---> K- pi0 nu/tau) Using the BaBar Detector

    SciTech Connect

    Salvatore, F.; Lyon, A.J.; /Manchester U.

    2005-07-08

    A preliminary measurement of the branching fraction {Beta}({tau}{sup -} {yields} K{sup -}{pi}{sup 0}{nu}{sub {tau}}) is made using 124.4 fb{sup -1} of e{sup +}e{sup -} collision data provided by the PEP-II accelerator, operating primarily at {radical}s = 10.58 GeV, and recorded using the BABAR detector. They measure: {Beta}({tau}{sup -} {yields} K{sup -} {pi}{sup 0}{nu}{sub {tau}}) = (0.438 {+-} 0.004(stat) {+-} 0.022(syst))%. This result is the world's most precise measurement of this branching fraction to date and is consistent with the world average.

  14. Pseudophosphorylation of Tau at distinct epitopes or the presence of the P301L mutation targets the microtubule-associated protein Tau to dendritic spines.

    PubMed

    Xia, Di; Li, Chuanzhou; Götz, Jürgen

    2015-05-01

    Alzheimer's disease is characterized by the accumulation of amyloid-β (Aβ) and Tau in the brain. In mature neurons, Tau is concentrated in the axon and found at lower levels in the dendrite where it is required for targeting Fyn to the spines. Here Fyn mediates Aβ toxicity, which is vastly abrogated when Tau is either deleted or a truncated form of Tau (Tau(1-255)) is co-expressed. Interestingly, MAP2, a microtubule-binding protein with mainly dendritic localization that shares Fyn-binding motifs with Tau, does not mediate Aβ's synaptic toxicity in the absence of Tau. Here we show in hippocampal neurons that endogenous Tau enters the entire spine, albeit at low levels, whereas MAP2 only enters its neck or is restricted to the dendritic shaft. Based on an extensive mutagenesis study, we also reveal that the spine localization of Tau is facilitated by deletion of the microtubule-binding repeat domain. When distinct phosphorylation sites (AT180-T231/S235, 12E8-S262/S356, PHF1-S396/S404) were pseudophosphorylated (with glutamic acid, using alanine replacements as controls), Tau targeting to spines was markedly increased, whereas the pseudophosphorylation of the late phospho-epitope S422 had no effect. In determining the role physiological Fyn has in the spine localization of Tau, we found that neither were endogenous Tau levels reduced in Fyn knockout compared with wild-type synaptosomal brain fractions nor was the spine localization of over-expressed pseudophosphorylated or P301L Tau. This demonstrates that although Fyn targeting to the spine is Tau dependent, elevated levels of phosphorylated Tau or P301L Tau can enter the spine in a Fyn-independent manner. PMID:25558816

  15. POLARIMETRY OF DG TAU AT 350 mum

    SciTech Connect

    Krejny, M.; Matthews, T. G.; Novak, G.; Cho, J.; Li, H.; Shinnaga, H.; Vaillancourt, J. E.

    2009-11-01

    We present the first 350 mum polarization measurement for the disk of the T Tauri star (TTS) DG Tau. The data were obtained using the SHARP polarimeter at the Caltech Submillimeter Observatory. We measured normalized Stokes parameters q= -0.0086 +- 0.0060 and u = -0.0012 +- 0.0061, which gives a 2sigma upper limit for the percent polarization of 1.7%. We obtain information about the polarization spectrum by comparing our 350 mum measurement with an 850 mum polarization detection previously published for this source. Comparing the two measurements in Stokes space (not in percent polarization) shows that the two data points are not consistent, i.e., either the degree of polarization or the angle of polarization (or both) must change significantly as one moves from 850 mum to 350 mum. This conclusion concerning the polarization spectrum disagrees with the predictions of a recent model for TTS disk polarization. We show that this discrepancy can be explained by optical depth effects. Specifically, we demonstrate that if one were to add more mass to the model disk, one would expect to obtain a model polarization spectrum in which the polarization degree falls sharply with increasing frequency, consistent with the observations at the two wavelengths. We suggest that multiwavelength polarimetry of TTS disk emission may provide a promising method for probing the opacity of TTS disks.

  16. Tau Pathology Spread in PS19 Tau Transgenic Mice Following Locus Coeruleus (LC) Injections of Synthetic Tau Fibrils is Determined by the LC’s Afferent and Efferent Connections

    PubMed Central

    Iba, Michiyo; McBride, Jennifer D.; Guo, Jing L.; Zhang, Bin; Trojanowski, John Q.; Lee, Virginia M.-Y.

    2015-01-01

    Filamentous tau inclusions are hallmarks of Alzheimer’s disease (AD) and other neurodegenerative tauopathies. An increasing number of studies implicate the cell-to-cell propagation of tau pathology in the progression of tauopathies. We recently showed [25] that inoculation of preformed synthetic tau fibrils (tau PFFs) into the hippocampus of young transgenic (Tg) mice (PS19) overexpressing human P301S mutant tau induced robust tau pathology in anatomically connected brain regions including the locus coeruleus (LC). Since Braak and colleagues hypothesized that the LC is the first brain structure to develop tau lesions and since LC has widespread connections throughout the CNS, LC neurons could be the critical initiators of the stereotypical spreading of tau pathology through connectome-dependent transmission of pathological tau in AD. Here, we report that injections of tau PFFs into the LC of PS19 mice induced propagation of tau pathology to major afferents and efferents of the LC. Notably, tau pathology propagated along LC efferent projections was localized not only to axon terminals but also to neuronal perikarya, suggesting transneuronal transfer of templated tau pathology to neurons receiving LC projections. Further, brainstem neurons giving rise to major LC afferents also developed perikaryal tau pathology. Surprisingly, while tangle bearing neurons degenerated in the LC ipsilateral to the injection site starting 6 months post-injection, no neuron loss was seen in the contralateral LC wherein tangle bearing neurons gradually cleared tau pathology by 6–12 months post-injection. However, the spreading pattern of tau pathology observed in our LC-injected mice is different from that in AD brains since hippocampus and entorhinal cortex, which are affected in early stages of AD, were largely spared of tau inclusions in our model. Thus, while our study tested critical aspects of the Braak hypothesis of tau pathology spread, this novel mouse model provides unique

  17. cuTauLeaping: A GPU-Powered Tau-Leaping Stochastic Simulator for Massive Parallel Analyses of Biological Systems

    PubMed Central

    Besozzi, Daniela; Pescini, Dario; Mauri, Giancarlo

    2014-01-01

    Tau-leaping is a stochastic simulation algorithm that efficiently reconstructs the temporal evolution of biological systems, modeled according to the stochastic formulation of chemical kinetics. The analysis of dynamical properties of these systems in physiological and perturbed conditions usually requires the execution of a large number of simulations, leading to high computational costs. Since each simulation can be executed independently from the others, a massive parallelization of tau-leaping can bring to relevant reductions of the overall running time. The emerging field of General Purpose Graphic Processing Units (GPGPU) provides power-efficient high-performance computing at a relatively low cost. In this work we introduce cuTauLeaping, a stochastic simulator of biological systems that makes use of GPGPU computing to execute multiple parallel tau-leaping simulations, by fully exploiting the Nvidia's Fermi GPU architecture. We show how a considerable computational speedup is achieved on GPU by partitioning the execution of tau-leaping into multiple separated phases, and we describe how to avoid some implementation pitfalls related to the scarcity of memory resources on the GPU streaming multiprocessors. Our results show that cuTauLeaping largely outperforms the CPU-based tau-leaping implementation when the number of parallel simulations increases, with a break-even directly depending on the size of the biological system and on the complexity of its emergent dynamics. In particular, cuTauLeaping is exploited to investigate the probability distribution of bistable states in the Schlögl model, and to carry out a bidimensional parameter sweep analysis to study the oscillatory regimes in the Ras/cAMP/PKA pathway in S. cerevisiae. PMID:24663957

  18. Tyrosine Nitration within the Proline-Rich Region of Tau in Alzheimer's Disease

    PubMed Central

    Reyes, Juan F.; Fu, Yifan; Vana, Laurel; Kanaan, Nicholas M.; Binder, Lester I.

    2011-01-01

    A substantial body of evidence suggests that nitrative injury contributes to neurodegeneration in Alzheimer's disease (AD) and other neurodegenerative disorders. Previously, we showed in vitro that within the tau protein the N-terminal tyrosine residues (Y18 and Y29) are more susceptible to nitrative modifications than other tyrosine sites (Y197 and Y394). Using site-specific antibodies to nitrated tau at Y18 and Y29, we identified tau nitrated in both glial (Y18) and neuronal (Y29) tau pathologies. In this study, we report the characterization of two novel monoclonal antibodies, Tau-nY197 and Tau-nY394, recognizing tau nitrated at Y197 and Y394, respectively. By Western blot analysis, Tau-nY197 labeled soluble tau and insoluble paired helical filament proteins (PHF-tau) nitrated at Y197 from control and AD brain samples. Tau-nY394 failed to label soluble tau isolated from control or severe AD samples, but labeled insoluble PHF-tau to a limited extent. Immunohistochemical analysis using Tau-nY197 revealed the hallmark tau pathology associated with AD; Tau-nY394 did not detect any pathological lesions characteristic of the disorder. These data suggest that a subset of the hallmark pathological inclusions of AD contain tau nitrated at Y197. However, nitration at Y197 was also identified in soluble tau from all control samples, including those at Braak stage 0, suggesting that nitration at this site in the proline-rich region of tau may have normal biological functions in the human brain. PMID:21514440

  19. Absence of a Role for Phosphorylation in the Tau Pathology of Alzheimer’s Disease

    PubMed Central

    Lai, Robert Y. K.; Harrington, Charles R.; Wischik, Claude M.

    2016-01-01

    Alzheimer’s disease is characterized by redistribution of the tau protein pool from soluble to aggregated states. Aggregation forms proteolytically stable core polymers restricted to the repeat domain, and this binding interaction has prion-like properties. We have compared the binding properties of tau and tubulin in vitro using a system in which we can measure binding affinities for proteins alternated between solid and aqueous phases. The study reveals that a phase-shifted repeat domain fragment from the Paired Helical Filament core contains all that is required for high affinity tau-tau binding. Unlike tau-tubulin binding, tau-tau binding shows concentration-dependent enhancement in both phase directions due to an avidity effect which permits one molecule to bind to many as the concentration in the opposite phase increases. Phosphorylation of tau inhibits tau-tau binding and tau-tubulin binding to equivalent extents. Tau-tau binding is favoured over tau-tubulin binding by factors in the range 19–41-fold, irrespective of phosphorylation status. A critical requirement for tau to become aggregation-competent is prior binding to a solid-phase substrate, which induces a conformational change in the repeat domain permitting high-affinity binding to occur even if tau is phosphorylated. The endogenous species enabling this nucleation event to occur in vivo remains to be identified. The findings of the study suggest that development of disease-modifying drugs for tauopathies should not target phosphorylation, but rather should target inhibitors of tau-tau binding or inhibitors of the binding interaction with as yet unidentified endogenous polyanionic substrates required to nucleate tau assembly. PMID:27070645

  20. Alzheimer’s Disease-Like Tau Neuropathology Leads to Memory Deficits and Loss of Functional Synapses in a Novel Mutated Tau Transgenic Mouse without Any Motor Deficits

    PubMed Central

    Schindowski, Katharina; Bretteville, Alexis; Leroy, Karelle; Bégard, Séverine; Brion, Jean-Pierre; Hamdane, Malika; Buée, Luc

    2006-01-01

    Tau transgenic mice are valuable models to investigate the role of tau protein in Alzheimer’s disease and other tauopathies. However, motor dysfunction and dystonic posture interfering with behavioral testing are the most common undesirable effects of tau transgenic mice. Therefore, we have generated a novel mouse model (THY-Tau22) that expresses human 4-repeat tau mutated at sites G272V and P301S under a Thy1.2-promotor, displaying tau pathology in the absence of any motor dysfunction. THY-Tau22 shows hyperphosphorylation of tau on several Alzheimer’s disease-relevant tau epitopes (AT8, AT100, AT180, AT270, 12E8, tau-pSer396, and AP422), neurofibrillary tangle-like inclusions (Gallyas and MC1-positive) with rare ghost tangles and PHF-like filaments, as well as mild astrogliosis. These mice also display deficits in hippocampal synaptic transmission and impaired behavior characterized by increased anxiety, delayed learning from 3 months, and reduced spatial memory at 10 months. There are no signs of motor deficits or changes in motor activity at any age investigated. This mouse model therefore displays the main features of tau pathology and several of the pathophysiological disturbances observed during neurofibrillary degeneration. This model will serve as an experimental tool in future studies to investigate mechanisms underlying cognitive deficits during pathogenic tau aggregation. PMID:16877359

  1. Evidence for the appearance of atmospheric tau neutrinos in super-Kamiokande.

    PubMed

    Abe, K; Hayato, Y; Iida, T; Iyogi, K; Kameda, J; Koshio, Y; Kozuma, Y; Marti, Ll; Miura, M; Moriyama, S; Nakahata, M; Nakayama, S; Obayashi, Y; Sekiya, H; Shiozawa, M; Suzuki, Y; Takeda, A; Takenaga, Y; Ueno, K; Ueshima, K; Yamada, S; Yokozawa, T; Ishihara, C; Kaji, H; Kajita, T; Kaneyuki, K; Lee, K P; McLachlan, T; Okumura, K; Shimizu, Y; Tanimoto, N; Labarga, L; Kearns, E; Litos, M; Raaf, J L; Stone, J L; Sulak, L R; Goldhaber, M; Bays, K; Kropp, W R; Mine, S; Regis, C; Renshaw, A; Smy, M B; Sobel, H W; Ganezer, K S; Hill, J; Keig, W E; Jang, J S; Kim, J Y; Lim, I T; Albert, J B; Scholberg, K; Walter, C W; Wendell, R; Wongjirad, T M; Ishizuka, T; Tasaka, S; Learned, J G; Matsuno, S; Smith, S N; Hasegawa, T; Ishida, T; Ishii, T; Kobayashi, T; Nakadaira, T; Nakamura, K; Nishikawa, K; Oyama, Y; Sakashita, K; Sekiguchi, T; Tsukamoto, T; Suzuki, A T; Takeuchi, Y; Ikeda, M; Minamino, A; Nakaya, T; Fukuda, Y; Itow, Y; Mitsuka, G; Tanaka, T; Jung, C K; Lopez, G D; Taylor, I; Yanagisawa, C; Ishino, H; Kibayashi, A; Mino, S; Mori, T; Sakuda, M; Toyota, H; Kuno, Y; Yoshida, M; Kim, S B; Yang, B S; Okazawa, H; Choi, Y; Nishijima, K; Koshiba, M; Yokoyama, M; Totsuka, Y; Martens, K; Schuemann, J; Vagins, M R; Chen, S; Heng, Y; Yang, Z; Zhang, H; Kielczewska, D; Mijakowski, P; Connolly, K; Dziomba, M; Thrane, E; Wilkes, R J

    2013-05-01

    Super-Kamiokande atmospheric neutrino data were fit with an unbinned maximum likelihood method to search for the appearance of tau leptons resulting from the interactions of oscillation-generated tau neutrinos in the detector. Relative to the expectation of unity, the tau normalization is found to be 1.42 ± 0.35(stat)(-0.12)(+0.14)(syst) excluding the no-tau-appearance hypothesis, for which the normalization would be zero, at the 3.8σ level. We estimate that 180.1 ± 44.3(stat)(-15.2)(+17.8) (syst) tau leptons were produced in the 22.5 kton fiducial volume of the detector by tau neutrinos during the 2806 day running period. In future analyses, this large sample of selected tau events will allow the study of charged current tau neutrino interaction physics with oscillation produced tau neutrinos. PMID:23683190

  2. Characterization of Early Pathological Tau Conformations and Phosphorylation in Chronic Traumatic Encephalopathy.

    PubMed

    Kanaan, Nicholas M; Cox, Kristine; Alvarez, Victor E; Stein, Thor D; Poncil, Sharra; McKee, Ann C

    2016-01-01

    Chronic traumatic encephalopathy (CTE) is a neurodegenerative tauopathy that develops after repetitive head injury. Several lines of evidence in other tauopathies suggest that tau oligomer formation induces neurotoxicity and that tau oligomer-mediated neurotoxicity involves induction of axonal dysfunction through exposure of an N-terminal motif in tau, the phosphatase-activating domain (PAD). Additionally, phosphorylation at serine 422 in tau occurs early and correlates with cognitive decline in patients with Alzheimer disease (AD). We performed immunohistochemistry and immunofluorescence on fixed brain sections and biochemical analysis of fresh brain extracts to characterize the presence of PAD-exposed tau (TNT1 antibody), tau oligomers (TOC1 antibody), tau phosphorylated at S422 (pS422 antibody), and tau truncated at D421 (TauC3 antibody) in the brains of 9-11 cases with CTE and cases of nondemented aged controls and AD (Braak VI) (n = 6, each). All 3 early tau markers (ie, TNT1, TOC1, and pS422) were present in CTE and displayed extensive colocalization in perivascular tau lesions that are considered diagnostic for CTE. Notably, the TauC3 epitope, which is abundant in AD, was relatively sparse in CTE. Together, these results provide the first description of PAD exposure, TOC1 reactive oligomers, phosphorylation of S422, and TauC3 truncation in the tau pathology of CTE. PMID:26671985

  3. Alzheimer’s disease imaging with a novel Tau targeted near infrared ratiometric probe

    PubMed Central

    Kim, Hye-Yeong; Sengupta, Urmi; Shao, Pin; Guerrero-Muñoz, Marcos J; Kayed, Rakez; Bai, Mingfeng

    2013-01-01

    Neurofibrillary tangles (NFTs) have long been recognized as one of the pathological hallmarks in Alzheimer’s disease (AD). Recent studies, however, showed that soluble aggregated Tau species, especially hyperphosphorylated Tau oligomers, which are formed at early stage of AD prior to the formation of NFT, disrupted neural system integration. Unfortunately, little is known about Tau aggregates, and few Tau targeted imaging probe has been reported. Successful development of new imaging methods that can visualize early stages of Tau aggregation specifically will obviously be important for AD imaging, as well as understanding Tau-associated neuropathology of AD. Here, we report the first NIR ratiometric probe, CyDPA2, that targets Tau aggregates. The specificity of CyPDA2 to aggregated Tau was evaluated with in vitro hyperphosphorylated Tau proteins (pTau), as well as ex vivo Tau samples from AD human brain samples and the tauopathy transgenic mouse model, P301L. The characteristic enhancements of absorption ratio and fluorescence intensity in CyDPA2 were observed in a pTau concentration-dependent manner. In addition, fluorescence microscopy and gel staining studies demonstrated CyDPA2-labeled Tau aggregates. These data indicate that CyDPA2 is a promising imaging probe for studying Tau pathology and diagnosing AD at an early stage. PMID:23526074

  4. Critical Role of Acetylation in Tau-Mediated Neurodegeneration and Cognitive Deficits

    PubMed Central

    Min, Sang-Won; Chen, Xu; Tracy, Tara E; Li, Yaqiao; Zhou, Yungui; Wang, Chao; Shirakawa, Kotaro; Minami, S. Sakura; Defensor, Erwin; Mok, Sue Ann; Sohn, Peter Dongmin; Schilling, Birgit; Cong, Xin; Ellerby, Lisa; Gibson, Bradford W.; Johnson, Jeffrey; Krogan, Nevan; Shamloo, Mehrdad; Gestwicki, Jason; Masliah, Eliezer; Verdin, Eric; Gan, Li

    2015-01-01

    Tauopathies, including frontotemporal dementia (FTD) and Alzheimer’s disease (AD), are neurodegenerative diseases in which tau fibrils accumulate. Recent evidence supports soluble tau species as the major toxic species. How soluble tau accumulates and how it causes neurodegeneration remains unclear. Here we identified tau acetylation at K174 as an early change in AD brains and as a critical determinant in tau homeostasis and toxicity in mice. An acetyl-mimicking mutant (K174Q) slows down tau turnover and induces cognitive deficits in vivo. The acetyltransferase p300-induced tau acetylation is inhibited by a prescription drug salsalate/salicylate, which enhances tau turnover and reduces tau levels. In the PS19 transgenic mouse model of FTD, administering salsalate after disease onset inhibited p300 activity, lowered ac-K174 and total tau levels, rescued tau-induced memory deficits and prevented hippocampal atrophy. The tau-lowering and protective effects of salsalate/salicylate are diminished in neurons expressing K174Q tau. Targeting tau acetylation could be a new therapeutic strategy against human tauopathies. PMID:26390242

  5. Planet formation in multiple stellar systems: GG Tau A

    NASA Astrophysics Data System (ADS)

    Di Folco, E.; Dutrey, A.; Guilloteau, S.; Le Bouquin, J.-B.; Lacour, S.; Berger, J.-P.; Köhler, R.; Piétu, V.

    2014-12-01

    GG Tau is a hierarchical quadruple system of young, low-mass stars. Because of its well-studied bright circumbinary ring of dust and gas surrounding the main binary GG Tau A, it is a unique laboratory to study planet formation in the disturbed environment of binary/multiple stellar systems. We have started a large observing program of GG Tau A that combines several high-resolution instruments in a multi-wavelength approach. We have recently reported the detection of a new low-mass companion in GG Tau A that turns out to itself be a triple system. This discovery was possible thanks to the very high angular resolution of the near-IR instrument PIONIER on the VLT interferometer, and was confirmed with sub-aperture masking techniques on VLT/NaCo. The detected close binary GG Tau Ab (ρ = 0.032'', or about 5 AU) provides a natural explanation for two enigmas: the discrepancy between the dynamical mass and the spectral type estimates in GG Tau A, and the absence of dust thermal emission in the vicinity of the Ab component. GRAVITY will provide the adequate angular resolution to complete the astrometric characterization of the close binary in the next 10 years. With now 5 coeval low-mass stars, GG Tau is an ideal laboratory to calibrate stellar evolution tracks at young ages (few Myr). Beyond this peculiar system, GRAVITY also has a strong potential to study the impact of multiplicity on the existence of disks, and in fine on planet formation mechanisms in multiple systems.

  6. ELISA measurement of specific antibodies to phosphorylated tau in intravenous immunoglobulin products.

    PubMed

    Loeffler, David A; Klaver, Andrea C; Coffey, Mary P

    2015-10-01

    The therapeutic effects of intravenous immunoglobulin (IVIG) products were recently studied in Alzheimer's disease (AD) patients. Pilot studies produced encouraging results but phase II and III trials gave disappointing results; a further study is in progress. IVIG products contain antibodies to tau protein, the main component of neurofibrillary tangles (NFTs). The tau used to detect IVIG's anti-tau antibodies in previous studies was non-phosphorylated recombinant human tau-441, but NFT-associated tau is extensively phosphorylated. The objective of this study was to determine if various IVIG products contain specific antibodies to phosphorylated tau (anti-pTau antibodies). ELISAs were used to evaluate binding of six IVIG products to a 12 amino acid peptide, tau 196-207, which was phosphorylated ("pTau peptide") or non-phosphorylated ("non-pTau peptide") at Serine-199 and Serine-202. Both amino acid residues are phosphorylated in AD NFTs. Each IVIG's "anti-pTau antibody ratio" was calculated by dividing its binding to the pTau peptide by its binding to the non-pTau peptide. Seven experiments were performed and data were pooled, with each experiment contributing one data point from each IVIG product. Mean anti-pTau antibody ratios greater than 1.0, suggesting specific antibodies to phosphorylated tau, were found for three IVIG products. Because administration of antibodies to phosphorylated tau has been found to reduce tau-associated pathology in transgenic mouse models of tauopathy, increasing the levels of anti-pTau antibodies, together with other selected antibodies such as anti-Aβ, in IVIG might increase its ability to slow AD's progression. PMID:26330100

  7. Observations of AA Tau requested to schedule XMM-Newton

    NASA Astrophysics Data System (ADS)

    Waagen, Elizabeth O.

    2013-08-01

    Dr. Hans Moritz Guenther (Harvard-Smithsonian Center for Astrophysics) has requested nightly observations of the classical T Tauri star AA Tau in order to schedule x-ray observations with XMM-Newton that have been planned for between 2013 August 15 and September 15. The purpose of the AAVSO observations is to determine whether AA Tau is at a suitable magnitude for the satellite observations. Taurus is difficult to observe during this time period but that is exactly why AAVSO assistance is needed! AA Tau is a morning object, and also, many of the professional ground-based telescopes are offline because of the US southwest monsoon season. Since it is critical to know the brightness of AA Tau, AAVSO observations will be truly essential. Nightly visual and snapshot (not more than once per night) observations beginning now and continuing through September 20 are needed. Coverage beginning ahead of the XMM window is requested because there is a one- to two-week lead time for the target to be inserted into the telescope schedule. Continuing the nightly observations a few days beyond the end of the XMM window will give better optical context for the x-ray data. AA Tau ranges between ~12.8V and ~16.1V; since December 2011 or earlier it has been at ~14.5V. The most recent observation in the AAVSO International Database shows it at 14.779V on 2013 Feb 5 (J. Roe, Bourbon, MO). Dr. Guenther writes, "AA Tau is surrounded by a thick accretion disk which is seen nearly edge-on. For decades the light curve of AA Tau showed regular eclipsing events when the accretion funnel rotated through the line of sight. However, earlier this year J. Bouvier and his group found that this behavior changed dramatically: AA Tau now seems to be deeply absorbed all the time (V band 14.5 mag). In collaboration with this group we will perform X-ray observations of AA Tau with the XMM-Newton satellite." Finder charts with sequence may be created using the AAVSO Variable Star Plo! tter (http

  8. Multinomial tau-leaping method for stochastic kinetic simulations.

    PubMed

    Pettigrew, Michel F; Resat, Haluk

    2007-02-28

    We introduce the multinomial tau-leaping (MtauL) method for general reaction networks with multichannel reactant dependencies. The MtauL method is an extension of the binomial tau-leaping method where efficiency is improved in several ways. First, tau-leaping steps are determined simply and efficiently using a priori information and Poisson distribution-based estimates of expectation values for reaction numbers over a tentative tau-leaping step. Second, networks are partitioned into closed groups of reactions and corresponding reactants in which no group reactant set is found in any other group. Third, product formation is factored into upper-bound estimation of the number of times a particular reaction occurs. Together, these features allow larger time steps where the numbers of reactions occurring simultaneously in a multichannel manner are estimated accurately using a multinomial distribution. Furthermore, we develop a simple procedure that places a specific upper bound on the total reaction number to ensure non-negativity of species populations over a single multiple-reaction step. Using two disparate test case problems involving cellular processes--epidermal growth factor receptor signaling and a lactose operon model--we show that the tau-leaping based methods such as the MtauL algorithm can significantly reduce the number of simulation steps thus increasing the numerical efficiency over the exact stochastic simulation algorithm by orders of magnitude. PMID:17343434

  9. Oligomerization of the protein tau in the Alzheimer's disease

    NASA Astrophysics Data System (ADS)

    Larini, Luca

    The Alzheimer's disease is characterized by the formation of protein aggregates both within and outside of the brain's cells, the neurons. Within the neurons, the aggregation of the microtubule associated protein tau leads to the destruction of the microtubules in the axon of the neuron. Tau is extremely flexible and is classified as an intrinsically disordered protein due to its low propensity to form secondary structure. Tau promotes tubulin assembly into microtubules, which are an essential component of the cytoskeleton of the axon. The microtubule binding region of tau consists of 4 pseudo-repeats that are critical for aggregation as well. In this study, we focus on the aggregation propensity of different segments of the microtubule binding region as well as post-translational modifications that can alter tau dynamics and structure. We have performed replica exchange molecular dynamics simulations to characterize the ensemble of conformations of the monomer and small oligomers as well as how these structures are stabilized or destabilized by mutations and post-translational modifications.

  10. Oligomer Formation of Tau Protein Hyperphosphorylated in Cells*

    PubMed Central

    Tepper, Katharina; Biernat, Jacek; Kumar, Satish; Wegmann, Susanne; Timm, Thomas; Hübschmann, Sabrina; Redecke, Lars; Mandelkow, Eva-Maria; Müller, Daniel J.; Mandelkow, Eckhard

    2014-01-01

    Abnormal phosphorylation (“hyperphosphorylation”) and aggregation of Tau protein are hallmarks of Alzheimer disease and other tauopathies, but their causative connection is still a matter of debate. Tau with Alzheimer-like phosphorylation is also present in hibernating animals, mitosis, or during embryonic development, without leading to pathophysiology or neurodegeneration. Thus, the role of phosphorylation and the distinction between physiological and pathological phosphorylation needs to be further refined. So far, the systematic investigation of highly phosphorylated Tau was difficult because a reliable method of preparing reproducible quantities was not available. Here, we generated full-length Tau (2N4R) in Sf9 cells in a well defined phosphorylation state containing up to ∼20 phosphates as judged by mass spectrometry and Western blotting with phospho-specific antibodies. Despite the high concentration in living Sf9 cells (estimated ∼230 μm) and high phosphorylation, the protein was not aggregated. However, after purification, the highly phosphorylated protein readily formed oligomers, whereas fibrils were observed only rarely. Exposure of mature primary neuronal cultures to oligomeric phospho-Tau caused reduction of spine density on dendrites but did not change the overall cell viability. PMID:25339173

  11. P70 S6 kinase mediates tau phosphorylation and synthesis.

    PubMed

    Pei, Jin-Jing; An, Wen-Lin; Zhou, Xin-Wen; Nishimura, Takeshi; Norberg, Jan; Benedikz, Eirikur; Götz, Jürgen; Winblad, Bengt

    2006-01-01

    Currently, we found that the 70-kDa p70 S6 kinase (p70S6K) directly phosphorylates tau at S262, S214, and T212 sites in vitro. By immunoprecipitation, p-p70S6K (T421/S424) showed a close association with p-tau (S262 and S396/404). Zinc-induced p70S6K activation could only upregulate translation of total S6 and tau but not global proteins in SH-SY5Y cells. The requirement of p70S6K activation was confirmed in the SH-SY5Y cells that overexpress wild-type htau40. Level of p-p70S6K (T421/S424) was only significantly correlated with p-tau at S262, S214, and T212, but not T212/S214, in Alzheimer's disease (AD) brains. These suggested that p70S6K might contribute to tau related pathologies in AD brains. PMID:16364302

  12. TauG-guidance of transients in expressive musical performance.

    PubMed

    Schogler, Benjaman; Pepping, Gert-Jan; Lee, David N

    2008-08-01

    The sounds in expressive musical performance, and the movements that produce them, offer insight into temporal patterns in the brain that generate expression. To gain understanding of these brain patterns, we analyzed two types of transient sounds, and the movements that produced them, during a vocal duet and a bass solo. The transient sounds studied were inter-tone f (0)(t)-glides (the continuous change in fundamental frequency, f (0)(t), when gliding from one tone to the next), and attack intensity-glides (the continuous rise in sound intensity when attacking, or initiating, a tone). The temporal patterns of the inter-tone f (0)(t)-glides and attack intensity-glides, and of the movements producing them, all conformed to the mathematical function, tau (G)(t) (called tauG), predicted by General Tau Theory, and assumed to be generated in the brain. The values of the parameters of the tau (G)(t) function were modulated by the performers when they modulated musical expression. Thus the tau (G)(t) function appears to be a fundamental of brain activity entailed in the generation of expressive temporal patterns of movement and sound. PMID:18560815

  13. 3D Visualization of the Temporal and Spatial Spread of Tau Pathology Reveals Extensive Sites of Tau Accumulation Associated with Neuronal Loss and Recognition Memory Deficit in Aged Tau Transgenic Mice

    PubMed Central

    Fu, Hongjun; Hussaini, S. Abid; Wegmann, Susanne; Profaci, Caterina; Daniels, Jacob D.; Herman, Mathieu; Emrani, Sheina; Figueroa, Helen Y.; Hyman, Bradley T.; Davies, Peter; Duff, Karen E.

    2016-01-01

    3D volume imaging using iDISCO+ was applied to observe the spatial and temporal progression of tau pathology in deep structures of the brain of a mouse model that recapitulates the earliest stages of Alzheimer’s disease (AD). Tau pathology was compared at four timepoints, up to 34 months as it spread through the hippocampal formation and out into the neocortex along an anatomically connected route. Tau pathology was associated with significant gliosis. No evidence for uptake and accumulation of tau by glia was observed. Neuronal cells did appear to have internalized tau, including in extrahippocampal areas as a small proportion of cells that had accumulated human tau protein did not express detectible levels of human tau mRNA. At the oldest timepoint, mature tau pathology in the entorhinal cortex (EC) was associated with significant cell loss. As in human AD, mature tau pathology in the EC and the presence of tau pathology in the neocortex correlated with cognitive impairment. 3D volume imaging is an ideal technique to easily monitor the spread of pathology over time in models of disease progression. PMID:27466814

  14. 3D Visualization of the Temporal and Spatial Spread of Tau Pathology Reveals Extensive Sites of Tau Accumulation Associated with Neuronal Loss and Recognition Memory Deficit in Aged Tau Transgenic Mice.

    PubMed

    Fu, Hongjun; Hussaini, S Abid; Wegmann, Susanne; Profaci, Caterina; Daniels, Jacob D; Herman, Mathieu; Emrani, Sheina; Figueroa, Helen Y; Hyman, Bradley T; Davies, Peter; Duff, Karen E

    2016-01-01

    3D volume imaging using iDISCO+ was applied to observe the spatial and temporal progression of tau pathology in deep structures of the brain of a mouse model that recapitulates the earliest stages of Alzheimer's disease (AD). Tau pathology was compared at four timepoints, up to 34 months as it spread through the hippocampal formation and out into the neocortex along an anatomically connected route. Tau pathology was associated with significant gliosis. No evidence for uptake and accumulation of tau by glia was observed. Neuronal cells did appear to have internalized tau, including in extrahippocampal areas as a small proportion of cells that had accumulated human tau protein did not express detectible levels of human tau mRNA. At the oldest timepoint, mature tau pathology in the entorhinal cortex (EC) was associated with significant cell loss. As in human AD, mature tau pathology in the EC and the presence of tau pathology in the neocortex correlated with cognitive impairment. 3D volume imaging is an ideal technique to easily monitor the spread of pathology over time in models of disease progression. PMID:27466814

  15. Passive immunization targeting the N-terminal projection domain of tau decreases tau pathology and improves cognition in a transgenic mouse model of Alzheimer disease and tauopathies.

    PubMed

    Dai, Chun-ling; Chen, Xia; Kazim, Syed Faraz; Liu, Fei; Gong, Cheng-Xin; Grundke-Iqbal, Inge; Iqbal, Khalid

    2015-04-01

    Intraneuronal accumulation of abnormally hyperphosphorylated tau in the brain is a histopathological hallmark of Alzheimer's disease and a family of related neurodegenerative disorders collectively called tauopathies. At present there is no effective treatment available for these progressive neurodegenerative diseases which are clinically characterized by dementia in mid to old-age. Here we report the treatment of 14-17-months-old 3xTg-AD mice with tau antibodies 43D (tau 6-18) and 77E9 (tau 184-195) to the N-terminal projection domain of tau or mouse IgG as a control by intraperitoneal injection once a week for 4 weeks, and the effects of the passive immunization on reduction of hyperphosphorylated tau, Aβ accumulation and cognitive performance in these animals. We found that treatment with tau antibodies 43D and 77E9 reduced total tau level, decreased tau hyperphosphorylated at Ser199, Ser202/Thr205 (AT8), Thr205, Ser262/356 (12E8), and Ser396/404 (PHF-1) sites, and a trend to reduce Aβ pathology. Most importantly, targeting N-terminal tau especially by 43D (tau 6-18) improved reference memory in the Morris water maze task in 3xTg-AD mice. We did not observe any abnormality in general physical characteristics of the treated animals with either of the two antibodies during the course of this study. Taken together, our studies demonstrate for the first time (1) that passive immunization targeting normal tau can effectively clear the hyperphosphorylated protein and possibly reduce Aβ pathology from the brain and (2) that targeting N-terminal projection domain of tau containing amino acid 6-18 is especially beneficial. Thus, targeting selective epitopes of N-terminal domain of tau may present a novel effective therapeutic opportunity for Alzheimer disease and other tauopathies. PMID:25233799

  16. Monitoring of Intracellular Tau Aggregation Regulated by OGA/OGT Inhibitors.

    PubMed

    Lim, Sungsu; Haque, Md Mamunul; Nam, Ghilsoo; Ryoo, Nayeon; Rhim, Hyewhon; Kim, Yun Kyung

    2015-01-01

    Abnormal phosphorylation of tau has been considered as a key pathogenic mechanism inducing tau aggregation in multiple neurodegenerative disorders, collectively called tauopathies. Recent evidence showed that tau phosphorylation sites are protected with O-linked β-N-acetylglucosamine (O-GlcNAc) in normal brain. In pathological condition, tau is de-glycosylated and becomes a substrate for kinases. Despite the importance of O-GlcNAcylation in tau pathology, O-GlcNAc transferase (OGT), and an enzyme catalyzing O-GlcNAc to tau, has not been carefully investigated in the context of tau aggregation. Here, we investigated intracellular tau aggregation regulated by BZX2, an inhibitor of OGT. Upon the inhibition of OGT, tau phosphorylation increased 2.0-fold at Ser199 and 1.5-fold at Ser396, resulting in increased tau aggregation. Moreover, the BZX2 induced tau aggregation was efficiently reduced by the treatment of Thiamet G, an inhibitor of O-GlcNAcase (OGA). Our results demonstrated the protective role of OGT in tau aggregation and also suggest the counter-regulatory mechanism of OGA and OGT in tau pathology. PMID:26343633

  17. Monitoring of Intracellular Tau Aggregation Regulated by OGA/OGT Inhibitors

    PubMed Central

    Lim, Sungsu; Haque, Md. Mamunul; Nam, Ghilsoo; Ryoo, Nayeon; Rhim, Hyewhon; Kim, Yun Kyung

    2015-01-01

    Abnormal phosphorylation of tau has been considered as a key pathogenic mechanism inducing tau aggregation in multiple neurodegenerative disorders, collectively called tauopathies. Recent evidence showed that tau phosphorylation sites are protected with O-linked β-N-acetylglucosamine (O-GlcNAc) in normal brain. In pathological condition, tau is de-glycosylated and becomes a substrate for kinases. Despite the importance of O-GlcNAcylation in tau pathology, O-GlcNAc transferase (OGT), and an enzyme catalyzing O-GlcNAc to tau, has not been carefully investigated in the context of tau aggregation. Here, we investigated intracellular tau aggregation regulated by BZX2, an inhibitor of OGT. Upon the inhibition of OGT, tau phosphorylation increased 2.0-fold at Ser199 and 1.5-fold at Ser396, resulting in increased tau aggregation. Moreover, the BZX2 induced tau aggregation was efficiently reduced by the treatment of Thiamet G, an inhibitor of O-GlcNAcase (OGA). Our results demonstrated the protective role of OGT in tau aggregation and also suggest the counter-regulatory mechanism of OGA and OGT in tau pathology. PMID:26343633

  18. Sustained high levels of neuroprotective, high molecular weight, phosphorylated tau in the longest-lived rodent

    PubMed Central

    Orr, Miranda E.; Garbarino, Valentina R.; Salinas, Angelica; Buffenstein, Rochelle

    2016-01-01

    Tau protein is primarily expressed in neuronal axons and modulates microtubule stability. Tau phosphorylation, aggregation and subcellular mislocalization coincide with neurodegeneration in numerous diseases, including Alzheimer's disease [AD]. During AD pathogenesis, tau misprocessing accompanies Aß accumulation; however, AD animal models, despite elevated Aß, fail to develop tauopathy. To assess whether lack of tau pathology is linked to short lifespan common to most AD models, we examined tau processing in extraordinarily long-lived, mouse-sized naked mole-rats (NMR; ~32 years), which express appreciable levels of Aß throughout life. NMRs, like other mammals, displayed highest tau phosphorylation during brain development. While tau phosphorylation decreased with aging, unexpectedly adult NMRs had higher levels than transgenic mice overexpressing mutant human tau. However, in sharp contrast with the somatodendritic accumulation of misprocessed tau in the transgenic mice, NMRs maintain axonal tau localization. Intriguingly, the adult NMR tau protein is 88kDa, much larger than 45-68kDa tau expressed in other mammals. We propose that this 88kDa tau protein may offer exceptional microtubule stability and neuroprotection against lifelong elevated Aß. PMID:25576082

  19. HS3ST2 expression is critical for the abnormal phosphorylation of tau in Alzheimer's disease-related tau pathology.

    PubMed

    Sepulveda-Diaz, Julia Elisa; Alavi Naini, Seyedeh Maryam; Huynh, Minh Bao; Ouidja, Mohand Ouidir; Yanicostas, Constantin; Chantepie, Sandrine; Villares, Joao; Lamari, Foudil; Jospin, Estelle; van Kuppevelt, Toin H; Mensah-Nyagan, Ayikoe Guy; Raisman-Vozari, Rita; Soussi-Yanicostas, Nadia; Papy-Garcia, Dulce

    2015-05-01

    Heparan sulphate (glucosamine) 3-O-sulphotransferase 2 (HS3ST2, also known as 3OST2) is an enzyme predominantly expressed in neurons wherein it generates rare 3-O-sulphated domains of unknown functions in heparan sulphates. In Alzheimer's disease, heparan sulphates accumulate at the intracellular level in disease neurons where they co-localize with the neurofibrillary pathology, while they persist at the neuronal cell membrane in normal brain. However, it is unknown whether HS3ST2 and its 3-O-sulphated heparan sulphate products are involved in the mechanisms leading to the abnormal phosphorylation of tau in Alzheimer's disease and related tauopathies. Here, we first measured the transcript levels of all human heparan sulphate sulphotransferases in hippocampus of Alzheimer's disease (n = 8; 76.8 ± 3.5 years old) and found increased expression of HS3ST2 (P < 0.001) compared with control brain (n = 8; 67.8 ± 2.9 years old). Then, to investigate whether the membrane-associated 3-O-sulphated heparan sulphates translocate to the intracellular level under pathological conditions, we used two cell models of tauopathy in neuro-differentiated SH-SY5Y cells: a tau mutation-dependent model in cells expressing human tau carrying the P301L mutation hTau(P301L), and a tau mutation-independent model in where tau hyperphosphorylation is induced by oxidative stress. Confocal microscopy, fluorescence resonance energy transfer, and western blot analyses showed that 3-O-sulphated heparan sulphates can be internalized into cells where they interact with tau, promoting its abnormal phosphorylation, but not that of p38 or NF-κB p65. We showed, in vitro, that the 3-O-sulphated heparan sulphates bind to tau, but not to GSK3B, protein kinase A or protein phosphatase 2, inducing its abnormal phosphorylation. Finally, we demonstrated in a zebrafish model of tauopathy expressing the hTau(P301L), that inhibiting hs3st2 (also known as 3ost2) expression results in a strong inhibition of the

  20. Direct cellular delivery of human proteasomes to delay tau aggregation.

    PubMed

    Han, Dong Hoon; Na, Hee-Kyung; Choi, Won Hoon; Lee, Jung Hoon; Kim, Yun Kyung; Won, Cheolhee; Lee, Seung-Han; Kim, Kwang Pyo; Kuret, Jeff; Min, Dal-Hee; Lee, Min Jae

    2014-01-01

    The 26S proteasome is the primary machinery that degrades ubiquitin (Ub)-conjugated proteins, including many proteotoxic proteins implicated in neurodegeneraton. It has been suggested that the elevation of proteasomal activity is tolerable to cells and may be beneficial to prevent the accumulation of protein aggregates. Here we show that purified proteasomes can be directly transported into cells through mesoporous silica nanoparticle-mediated endocytosis. Proteasomes that are loaded onto nanoparticles through non-covalent interactions between polyhistidine tags and nickel ions fully retain their proteolytic activity. Cells treated with exogenous proteasomes are more efficient in degrading overexpressed human tau than endogenous proteasomal substrates, resulting in decreased levels of tau aggregates. Moreover, exogenous proteasome delivery significantly promotes cell survival against proteotoxic stress caused by tau and reactive oxygen species. These data demonstrate that increasing cellular proteasome activity through the direct delivery of purified proteasomes may be an effective strategy for reducing cellular levels of proteotoxic proteins. PMID:25476420

  1. Acetylated tau neuropathology in sporadic and hereditary tauopathies.

    PubMed

    Irwin, David J; Cohen, Todd J; Grossman, Murray; Arnold, Steven E; McCarty-Wood, Elisabeth; Van Deerlin, Vivianna M; Lee, Virginia M-Y; Trojanowski, John Q

    2013-08-01

    We have recently shown acetylation of tau at lysine residue 280 (AC-K280) to be a disease-specific modification in Alzheimer disease (AD), corticobasal degeneration, and progressive supranuclear palsy, likely representing a major regulatory tau modification. Herein, we extend our observations using IHC with a polyclonal antibody specific for AC-K280. Thirty brain regions were examined in argyrophilic grain disease (AGD; n = 5), tangle-predominant senile dementia (TPSD; n = 5), Pick disease (n = 4), familial AD (FAD; n = 2; PSEN1 p.G206A and p.S170P), and frontotemporal dementia with parkinsonism linked to chromosome-17 (FTDP-17; n = 2; MAPT p.P301L and IVS10 + 16). All AGD, TPSD, FAD, and FTDP-17 cases had significant AC-K280 reactivity that was similar in severity and distribution to phosphorylated tau. AC-K280 robustly labeled grain pathological characteristics in AGD and was predominantly associated with thioflavin-S-positive neurofibrillary tangles and less reactive in neuropil threads and extracellular tangles in TPSD and FAD. Thioflavin-S-negative neuronal and glial inclusions of patients with FTDP-17 were robustly AC-K280 reactive. A low degree of AC-K280 was found in a subset of 4-repeat tau-containing lesions in Pick disease. AC-K280 is a prominent feature of both neuronal and glial tau aggregations in tauopathies of various etiologies. The close association of AC-K280 with amyloid and pre-amyloid conformations of tau suggests a potential role in tangle maturation and, thus, could serve as a useful biomarker or therapeutic target in a variety of tauopathies. PMID:23885714

  2. Traceless purification and desulfurization of tau protein ligation products.

    PubMed

    Reimann, Oliver; Smet-Nocca, Caroline; Hackenberger, Christian P R

    2015-01-01

    We present a novel strategy for the traceless purification and synthetic modification of peptides and proteins obtained by native chemical ligation. The strategy involves immobilization of a photocleavable semisynthetic biotin-protein conjugate on streptavidin-coated agarose beads, which eliminates the need for tedious rebuffering steps and allows the rapid removal of excess peptides and additives. On-bead desulfurization is followed by delivery of the final tag-free protein product. The strategy is demonstrated in the isolation of a tag-free Alzheimer's disease related human tau protein from a complex EPL mixture as well as a triphosphorylated peptide derived from the C-terminus of tau. PMID:25404175

  3. Depletion of microglia and inhibition of exosome synthesis halt tau propagation.

    PubMed

    Asai, Hirohide; Ikezu, Seiko; Tsunoda, Satoshi; Medalla, Maria; Luebke, Jennifer; Haydar, Tarik; Wolozin, Benjamin; Butovsky, Oleg; Kügler, Sebastian; Ikezu, Tsuneya

    2015-11-01

    Accumulation of pathological tau protein is a major hallmark of Alzheimer's disease. Tau protein spreads from the entorhinal cortex to the hippocampal region early in the disease. Microglia, the primary phagocytes in the brain, are positively correlated with tau pathology, but their involvement in tau propagation is unknown. We developed an adeno-associated virus-based model exhibiting rapid tau propagation from the entorhinal cortex to the dentate gyrus in 4 weeks. We found that depleting microglia dramatically suppressed the propagation of tau and reduced excitability in the dentate gyrus in this mouse model. Moreover, we demonstrate that microglia spread tau via exosome secretion, and inhibiting ex