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Found 37769 matches. Displaying 7891-7900
Bettayeb K, Oumata N, Zhang YY, Luo WJ, Bustos V, Galons H, Greengard P, Meijer L, Flajolet M
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Small-molecule inducers of A beta-42 peptide production share a common mechanism of action
FASEB JOURNAL 2012 DEC; 26(12):5115-5123
The pathways leading specifically to the toxic A beta 42 peptide production, a key event in Alzheimer's disease (AD), are unknown. While searching for pathways that mediate pathological increases of A beta 42, we identified Aftin-4, a new compound that selectively and potently increases A beta 42 compared to DMSO (N2a cells: 7-fold; primary neurons: 4-fold; brain lysates: 2-fold) with an EC50 of 30 mu M. These results were confirmed by ELISA and IP-WB. Using affinity chromatography and mass spectrometry, we identified 3 proteins (VDAC1, prohibitin, and mitofilin) relevant to AD that interact with Aftin-4, but not with a structurally similar but inactive molecule. Electron microscopy studies demonstrated that Aftin-4 induces a reversible mitochondrial phenotype reminiscent of the one observed in AD brains. Sucrose gradient fractionation showed that Aftin-4 perturbs the subcellular localization of gamma-secretase components and could, therefore, modify gamma-secretase specificity by locally altering its membrane environment. Remarkably, Aftin-4 shares all these properties with two other "AD accelerator" compounds. In summary, treatment with three A beta 42 raising agents induced similar biochemical alterations that lead to comparable cellular phenotypes in vitro, suggesting a common mechanism of action involving three structural cellular targets.-Bettayeb, K., Oumata, N., Zhang, Y., Luo, W., Bustos, V., Galons, H., Greengard, P., Meijer, L., Flajolet, M. Small-molecule inducers of A beta-42 peptide production share a common mechanism of action. FASEB J. 26, 5115-5123 (2012). www.fasebj.org
Weller S, Bonnet M, Delagreverie H, Israel L, Chrabieh M, Marodi L, Rodriguez-Gallego C, Garty BZ, Roifman C, Issekutz AC, Zitnik SE, Hoarau C, Camcioglu Y, Vasconcelos J, Rodrigo C, Arkwright PD, Cerutti A, Meffre E, Zhang SY, Alcais A, Puel A, Casanova JL, Picard C, Weill JC, Reynaud CA
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IgM(+)IgD(+)CD27(+)B cells are markedly reduced in IRAK-4-, MyD88-, and TIRAP- but not UNC-93B-deficient patients
BLOOD 2012 DEC 13; 120(25):4992-5001
We studied the distribution of peripheral B-cell subsets in patients deficient for key factors of the TLR-signaling pathways (MyD88, TIRAP/MAL, IL-1 receptor-associated kinase 4 [IRAK-4], TLR3, UNC-93B, TRIF). All TLRs, except TLR3, which signals through the TRIF adaptor, require MyD88 and IRAK-4 to mediate their function. TLR4 and the TLR2 heterodimers (with TLR1, TLR6, and possibly TLR10) require in addition the adaptor TIRAP, whereas UNC-93B is needed for the proper localization of intracellular TLR3, TLR7, TLR8, and TLR9. We found that IgM(+)IgD(+)CD27(+) but not switched B cells were strongly reduced in MyD88-, IRAK-4-, and TIRAP-deficient patients. This defect did not appear to be compensated with age. However, somatic hypermutation of Ig genes and heavy-chain CDR3 size distribution of IgM(+)IgD(+)CD27(+)B cells were not affected in these patients. In contrast, the numbers of IgM(+)IgD(+)CD27(+)B cells were normal in the absence of TLR3, TRIF, and UNC-93B, suggesting that UNC-93B-dependent TLRs, and notably TLR9, are dispensable for the presence of this subset in peripheral blood. Interestingly, TLR10 was found to be expressed at greater levels in IgM(+)IgD(+)CD27(+) compared with switched B cells in healthy patients. Hence, we propose a role for TIRAP-dependent TLRs, possibly TLR10 in particular, in the development and/or maintenance of IgM(+)IgD(+)CD27(+)B cells in humans. (Blood. 2012; 120(25): 4992-5001)
Fava V, Orlova M, Cobat A, Alcais A, Mira M, Schurr E
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Genetics of leprosy reactions: an overview
MEMORIAS DO INSTITUTO OSWALDO CRUZ 2012 DEC; 107(?):132-142
Type-1 (T1R) and Type-2 (T2R) leprosy reactions (LR), which affect up to 50% of leprosy patients, are aggressive inflammatory episodes of sudden onset and highly variable incidence across populations. LR are often diagnosed concurrently with leprosy, but more frequently occur several months after treatment onset. It is not uncommon for leprosy patients to develop recurring reactional episodes; however, they rarely undergo both types of LR. Today, LR are the main cause of permanent disabilities associated with leprosy and represent a major challenge in the clinical management of leprosy patients. Although progress has been made in understanding the immunopathology of LR, the factors that cause a leprosy patient to suffer from LR are largely unknown. Given the impact that ethnic background has on the risk of developing LR, host genetic factors have long been suspected of contributing to LR. Indeed, polymorphisms in seven genes [Toll-like receptors (TLR)1, TLR2, nucleotide-b!
Nin F, Reichenbach T, Fisher JAN, Hudspeth AJ
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Contribution of active hair-bundle motility to nonlinear amplification in the mammalian cochlea
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA 2012 DEC 18; 109(51):21076-21080
The cochlea's high sensitivity stems from the active process of outer hair cells, which possess two force-generating mechanisms: active hair-bundle motility elicited by Ca2+ influx and somatic motility mediated by the voltage-sensitive protein prestin. Although interference with prestin has demonstrated a role for somatic motility in the active process, it remains unclear whether hair-bundle motility contributes in vivo. We selectively perturbed the two mechanisms by infusing substances into the endolymph or perilymph of the chinchilla's cochlea and then used scanning laser interferometry to measure vibrations of the basilar membrane. Blocking somatic motility, damaging the tip links of hair bundles, or depolarizing hair cells eliminated amplification. While reducing amplification to a lesser degree, pharmacological perturbation of active hair-bundle motility diminished or eliminated the nonlinear compression underlying the broad dynamic range associated with normal hearing. The results suggest that active hair-bundle motility plays a significant role in the amplification and compressive nonlinearity of the cochlea.
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Rios AAO, Ryckbosch D, Strobbe N, Thyssen F, Tytgat M, Verwilligen P, Walsh S, Yazgan E, Zaganidis N, Basegmez S, Bruno G, Castello R, Ceard L, Delaere C, du Pree T, Favart D, Forthomme L, Giammanco A, Hollar J, Lemaitre V, Liao J, Militaru O, Nuttens C, Pagano D, Pin A, Piotrzkowski K, Schul N, Garcia JMV, Beliy N, Caebergs T, Daubie E, Hammad GH, Alves GA, Martins MC, Damiao DDJ, Martins T, Pol ME, Souza MHG, Alda WL, Carvalho W, Custodio A, Da Costa EM, Martins CDO, De Souza SF, Figueiredo DM, Mundim L, Nogima H, Oguri V, Da Silva WLP, Santoro A, Jorge LS, Sznajder A, Bernardes CA, Dias FA, Tomei TRFP, Gregores EM, Lagana C, Marinho F, Mercadante PG, Novaes SF, Padula SS, Genchev V, Iaydjiev P, Piperov S, Rodozov M, Stoykova S, Sultanov G, Tcholakov V, Trayanov R, Vutova M, Dimitrov A, Hadjiiska R, Kozhuharov V, Litov L, Pavlov B, Petkov P, Bian JG, Chen GM, Chen HS, Jiang CH, Liang D, Liang S, Meng X, Tao J, Wang J, Wang X, Wang Z, Xiao H, Xu M, Zang J, Zhang Z, Asawatangtrakuldee C, Ban Y, Guo S, Guo Y, Li W, Liu S, Mao Y, Qian SJ, Teng H, Wang D, Zhang L, Zhu B, Zou W, Avila C, Gomez JP, Moreno BG, Oliveros AFO, Sanabria JC, Godinovic N, Lelas D, Plestina R, Polic D, Puljak I, Antunovic Z, Kovac M, Brigljevic V, Duric S, Kadija K, Luetic J, Morovic S, Attikis A, Galanti M, Mavromanolakis G, Mousa J, Nicolaou C, Ptochos F, Razis PA, Finger M, Finger M, Assran Y, Elgammal S, Kamel AE, Mahmoud MA, Radi A, Kadastik M, Muntel M, Raidal M, Rebane L, Tiko A, Eerola P, Fedi G, Voutilainen M, Harkonen J, Heikkinen A, Karimaki V, Kinnunen R, Kortelainen MJ, Lampen T, Lassila-Perini K, Lehti S, Linden T, Luukka P, Maenpaa T, Peltola T, Tuominen E, Tuominiemi J, Tuovinen E, Ungaro D, Wendland L, Banzuzi K, Karjalainen A, Korpela A, Tuuva T, Besancon M, Choudhury S, Dejardin M, Denegri D, Fabbro B, Faure JL, Ferri F, Ganjour S, Givernaud A, Gras P, de Monchenault GH, Jarry P, Locci E, Malcles J, Millischer L, Nayak A, Rander J, Rosowsky A, Shreyber I, Titov M, Baffioni S, Beaudette F, Benhabib L, Bianchini L, Bluj M, Broutin C, Busson P, Charlot C, Daci N, Dahms T, Dobrzynski L, de Cassagnac RG, Haguenauer M, Mine P, Mironov C, Nguyen M, Ochando C, Paganini P, Sabes D, Salerno R, Sirois Y, Veelken C, Zabi A, Agram JL, Andrea J, Bloch D, Bodin D, Brom JM, Cardaci M, Chabert EC, Collard C, Conte E, Drouhin F, Ferro C, Fontaine JC, Gele D, Goerlach U, Juillot P, Le Bihan AC, Van Hove P, Fassi F, Mercier D, Beauceron S, Beaupere N, Bondu O, Boudoul G, Chasserat J, Chierici R, Contardo D, Depasse P, El Mamouni H, Fay J, Gascon S, Gouzevitch M, Ille B, Kurca T, Lethuillier M, Mirabito L, Perries S, Sordini V, Tosi S, Tschudi Y, Verdier P, Viret S, Tsamalaidze Z, Anagnostou G, Beranek S, Edelhoff M, Feld L, Heracleous N, Hindrichs O, Jussen R, Klein K, Merz J, Ostapchuk A, Perieanu A, Raupach F, Sammet J, Schael S, Sprenger D, Weber H, Wittmer B, Zhukov V, Ata M, Caudron J, Dietz-Laursonn E, Duchardt D, Erdmann M, Fischer R, Guth A, Hebbeker T, Heidemann C, Hoepfner K, Klingebiel D, Kreuzer P, Lingemann J, Magass C, Merschmeyer M, Meyer A, Olschewski M, Papacz P, Pieta H, Reithler H, Schmitz SA, Sonnenschein L, Steggemann J, Teyssier D, Weber M, Bontenackels M, Cherepanov V, Flugge G, Geenen H, Geisler M, Ahmad WH, Hoehle F, Kargoll B, Kress T, Kuessel Y, Nowack A, Perchalla L, Pooth O, Rennefeld J, Sauerland P, Stahl A, Martin MA, Behr J, Behrenhoff W, Behrens U, Bergholz M, Bethani A, Borras K, Burgmeier A, Cakir A, Calligaris L, Campbell A, Castro E, Costanza F, Dammann D, Pardos CD, Eckerlin G, Eckstein D, Flucke G, Geiser A, Glushkov I, Gunnellini P, Habib S, Hauk J, Hellwig G, Jung H, Kasemann M, Katsas P, Kleinwort C, Kluge H, Knutsson A, Kramer M, Krucker D, Kuznetsova E, Lange W, Lohmann W, Lutz B, Mankel R, Marfin I, Marienfeld M, Melzer-Pellmann IA, Meyer AB, Mnich J, Mussgiller A, Naumann-Emme S, Olzem J, Perrey H, Petrukhin A, Pitzl D, Raspereza A, Cipriano PMR, Riedl C, Ron E, Rosin M, Salfeld-Nebgen J, Schmidt R, 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Mavrommatis C, Ntomari E, Gouskos L, Mertzimekis TJ, Panagiotou A, Saoulidou N, Evangelou I, Foudas C, Kokkas P, Manthos N, Papadopoulos I, Patras V, Bencze G, Hajdu C, Hidas P, Horvath D, Sikler F, Veszpremi V, Vesztergombi G, Beni N, Czellar S, Molnar J, Palinkas J, Szillasi Z, Karancsi J, Raics P, Trocsanyi ZL, Ujvari B, Bansal M, Beri SB, Bhatnagar V, Dhingra N, Gupta R, Kaur M, Mehta MZ, Nishu N, Saini LK, Sharma A, Singh JB, Kumar A, Kumar A, Ahuja S, Bhardwaj A, Choudhary BC, Malhotra S, Naimuddin M, Ranjan K, Sharma V, Shivpuri RK, Banerjee S, Bhattacharya S, Dutta S, Gomber B, Jain S, Jain S, Khurana R, Sarkar S, Sharan M, Abdulsalam A, Choudhury RK, Dutta D, Kailas S, Kumar V, Mehta P, Mohanty AK, Pant LM, Shukla P, Aziz T, Ganguly S, Guchait M, Maity M, Majumder G, Mazumdar K, Mohanty GB, Parida B, Sudhakar K, Wickramage N, Banerjee S, Dugad S, Arfaei H, Bakhshiansohi H, Etesami SM, Fahim A, Hashemi M, Hesari H, Jafari A, Khakzad M, Najafabadi MM, Mehdiabadi SP, Safarzadeh B, Zeinali M, Abbrescia M, Barbone L, Calabria C, Chhibra SS, Colaleo A, Creanza D, De Filippis N, De Palma M, Fiore L, Iaselli G, Lusito L, Maggi G, Maggi M, Marangelli B, My S, Nuzzo S, Pacifico N, Pompili A, Pugliese G, Selvaggi G, Silvestris L, Singh G, Venditti R, Zito G, Abbiendi G, Benvenuti AC, Bonacorsi D, Braibant-Giacomelli S, Brigliadori L, Capiluppi P, Castro A, Cavallo FR, Cuffiani M, Dallavalle GM, Fabbri F, Fanfani A, Fasanella D, Giacomelli P, Grandi C, Guiducci L, Marcellini S, Masetti G, Meneghelli M, Montanari A, Navarria FL, Odorici F, Perrotta A, Primavera F, Rossi AM, Rovelli T, Siroli GP, Travaglini R, Albergo S, Cappello G, Chiorboli M, Costa S, Potenza R, Tricomi A, Tuve C, Barbagli G, Ciulli V, Civinini C, D'Alessandro R, Focardi E, Frosali S, Gallo E, Gonzi S, Meschini M, Paoletti S, Sguazzoni G, Tropiano A, Benussi L, Bianco S, Colafranceschi S, Fabbri F, Piccolo D, Fabbricatore P, Musenich R, Benaglia A, De Guio F, Di Matteo L, Fiorendi S, Gennai S, Ghezzi A, Malvezzi S, Manzoni RA, Martelli A, Massironi A, Menasce D, Moroni L, Paganoni M, Pedrini D, Ragazzi S, Redaelli N, Sala S, de Fatis TT, Buontempo S, Montoya CAC, Cavallo N, De Cosa A, Dogangun O, Fabozzi F, Iorio AOM, Lista L, Meola S, Merola M, Paolucci P, Azzi P, Bacchetta N, Bellato M, Bisello D, Branca A, Carlin R, Checchia P, Dorigo T, Gasparini F, Gasparini U, Gozzelino A, Kanishchev K, Lacaprara S, Lazzizzera I, Margoni M, Meneguzzo AT, Pazzini J, Pozzobon N, Ronchese P, Simonetto F, Torassa E, Tosi M, Vanini S, Zotto P, Zumerle G, Gabusi M, Ratti SP, Riccardi C, Torre P, Vitulo P, Biasini M, Bilei GM, Fano L, Lariccia P, Lucaroni A, Mantovani G, Menichelli M, Nappi A, Romeo F, Saha A, Santocchia A, Taroni S, Azzurri P, Bagliesi G, Bernardini J, Boccali T, Broccolo G, Castaldi R, D'Agnolo RT, Dell'Orso R, Fiori F, Foa L, Giassi A, Kraan A, Ligabue F, Lomtadze T, Martini L, Messineo A, Palla F, Rizzi A, Serban AT, Spagnolo P, Squillacioti P, Tenchini R, Tonelli G, Venturi A, Verdini PG, Barone L, Cavallari F, Del Re D, Diemoz M, Grassi M, Longo E, Meridiani P, Micheli F, Nourbakhsh S, Organtini G, Paramatti R, Rahatlou S, Sigamani M, Soffi L, Amapane N, Arcidiacono R, Argiro S, Arneodo M, Biino C, Cartiglia N, Costa M, Demaria N, Mariotti C, Maselli S, Mazza G, Migliore E, Monaco V, Musich M, Obertino MM, Pastrone N, Pelliccioni M, Potenza A, Romero A, Sacchi R, Solano A, Staiano A, Pereira AV, Belforte S, Candelise V, Cossutti F, Della Ricca G, Gobbo B, Marone M, Montanino D, Penzo A, Schizzi A, Heo SG, Kim TY, Nam SK, Chang S, Kim DH, Kim GN, Kong DJ, Park H, Ro SR, Son DC, Son T, Kim JY, Kim ZJ, Song S, Choi S, Gyun D, Hong B, Jo M, Kim H, Kim TJ, Lee KS, Moon DH, Park SK, Choi M, Kim JH, Park C, Park IC, Park S, Ryu G, Cho Y, Choi Y, Choi YK, Goh J, Kim MS, Kwon E, Lee B, Lee J, Lee S, Seo H, Yu I, Bilinskas MJ, Grigelionis I, Janulis M, Juodagalvis A, Castilla-Valdez H, De La Cruz-Burelo E, La Cruz IHD, Lopez-Fernandez R, Villalba RM, Martinez-Ortega J, Sanchez-Hernandez A, Villasenor-Cendejas LM, Moreno SC, Valencia FV, Ibarguen HAS, Linares EC, Pineda AM, Reyes-Santos MA, Krofcheck D, Bell AJ, Butler PH, Doesburg R, Reucroft S, Silverwood H, Ahmad M, Asghar MI, Hoorani HR, Khalid S, Khan WA, Khurshid T, Qazi S, Shah MA, Shoaib M, Bialkowska H, Boimska B, Frueboes T, Gokieli R, Gorski M, Kazana M, Nawrocki K, Romanowska-Rybinska K, Szleper M, Wrochna G, Zalewski P, Brona G, Bunkowski K, Cwiok M, Dominik W, Doroba K, Kalinowski A, Konecki M, Krolikowski J, Almeida N, Bargassa P, David A, Faccioli P, Parracho PGF, Gallinaro M, Seixas J, Varela J, Vischia P, Belotelov I, Gavrilenko M, Golutvin I, Kamenev A, Karjavin V, Konoplyanikov V, Kozlov G, Lanev A, Malakhov A, Moisenz P, Palichik V, Perelygin V, Savina M, Shmatov S, Smirnov V, Volodko A, Zarubin A, Evstyukhin S, Golovtsov V, Ivanov Y, Kim V, Levchenko P, Murzin V, Oreshkin V, Smirnov I, Sulimov V, Uvarov L, Vavilov S, Vorobyev A, Vorobyev A, Andreev Y, Dermenev A, Gninenko S, 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J, Lanaro A, Lazaridis C, Leonard J, Loveless R, Mohapatra A, Ojalvo I, Palmonari F, Pierro GA, Ross I, Savin A, Smith WH, Swanson J
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Observation of Z decays to four leptons with the CMS detector at the LHC
JOURNAL OF HIGH ENERGY PHYSICS 2012 DEC; ?(12):? Article 034
The first observation of the Z boson decaying to four leptons in proton-proton collisions is presented. The analyzed data set corresponds to an integrated luminosity of 5.02 fb(-1) at root s = 7 TeV collected by the CMS detector at the Large Hadron Collider. A pronounced resonance peak, with a statistical significance of 9.7 sigma, is observed in the distribution of the invariant mass of four leptons (electrons and/or muons) with mass and width consistent with expectations for Z boson decays. The branching fraction and cross section reported here are defined by phase space restrictions on the leptons, namely, 80 < m(4l) < 100 GeV, where m(4l) is the invariant mass of the four leptons, and m(ll) > 4 GeV for all pairs of leptons, where m(ll) is the two-lepton invariant mass. The measured branching fraction is B(Z -> 4(l)) = 4.2(-0.8)(+0.9)(stat.) +/- 0.2(syst.)) x 10(-6) and agrees with the standard model prediction of 4.45 x 10(-6). The measured cross section times branchi!
Ben-Dov IZ, Muthukumar T, Morozov P, Mueller FB, Tuschl T, Suthanthiran M
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MicroRNA Sequence Profiles of Human Kidney Allografts With or Without Tubulointerstitial Fibrosis
TRANSPLANTATION 2012 DEC 15; 94(11):1086-1094
Background. MicroRNA (miRNA) alterations accompanying interstitial fibrosis and tubular atrophy (IFTA) in kidney allografts may point toward pathologic mechanisms. Small-RNA sequencing provides information on total miRNA abundance and specific miRNA expression and allows analysis of differential expression based on read counts. Methods. MiRNA expression profiles of 8 human kidney allograft biopsies (4 IFTA and 4 normal biopsies, discovery set) were characterized using barcoded deep-sequencing of a cDNA library prepared from multiplexed RNA. Statistical analysis of the sequence data guided selection of miRNAs for validation and the levels of selected miRNAs were quantified in 18 biopsies (10 IFTA and 8 normal) using real-time quantitative PCR assays (RT-QPCR). Results. Total miRNA content was 50% lower in RNA from IFTA compared with normal biopsies. Global miRNA profiles clustered in partial agreement with diagnosis. Several miRNAs, including miR-21, 142-3p, and 5p and the cluster comprising miR-506 on chromosome X had twofold to sevenfold higher expression in IFTA compared with normal biopsies, whereas miRNA miR-30b and 30c were lower in IFTA biopsies (miR-30a, -30d, -30e, and all respective star sequences showed similar trends). IFTA and normal biopsy distinction was also noted in the pattern of miRNA nucleotide sequence variations. Differentially expressed miRNAs were confirmed on the larger set of allograft biopsies using RT-QPCR, and the levels of miRNAs were found to be associated with allograft function and survival. Conclusion. Differentially expressed miRNAs and their predicted targets identified by deep sequencing are candidates for further investigation to decipher the mechanism and management of kidney allograft fibrosis.
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Velicanu D, Wenger EA, Wolf R, Wyslouch B, Yang M, Yilmaz Y, Yoon AS, Zanetti M, Cooper SI, Dahmes B, De Benedetti A, Franzoni G, Gude A, Kao SC, Klapoetke K, Kubota Y, Mans J, Pastika N, Rusack R, Sasseville M, Singovsky A, Tambe N, Turkewitz J, Cremaldi LM, Kroeger R, Perera L, Rahmat R, Sanders DA, Avdeeva E, Bloom K, Bose S, Butt J, Claes DR, Dominguez A, Eads M, Keller J, Kravchenko I, Lazo-Flores J, Malbouisson H, Malik S, Snow GR, Baur U, Godshalk A, Iashvili I, Jain S, Kharchilava A, Kumar A, Shipkowski SP, Smith K, Alverson G, Barberis E, Baumgartel D, Chasco M, Haley J, Nash D, Trocino D, Wood D, Zhang J, Anastassov A, Kubik A, Mucia N, Odell N, Ofierzynski RA, Pollack B, Pozdnyakov A, Schmitt M, Stoynev S, Velasco M, Won S, Antonelli L, Berry D, Brinkerhoff A, Hildreth M, Jessop C, Karmgard DJ, Kolb J, Lannon K, Luo W, Lynch S, Marinelli N, Morse DM, Pearson T, Planer M, Ruchti R, Slaunwhite J, Valls N, Wayne M, Wolf M, Bylsma B, Durkin LS, Hill C, Hughes R, Hughes R, Kotov K, Ling TY, Puigh D, Rodenburg M, Vuosalo C, Williams G, Winer BL, Adam N, Berry E, Elmer P, Gerbaudo D, Halyo V, Hebda P, Hegeman J, Hunt A, Jindal P, Pegna DL, Lujan P, Marlow D, Medvedeva T, Mooney M, Olsen J, Piroue P, Quan X, Raval A, Safdi B, Saka H, Stickland D, Tully C, Werner JS, Zuranski A, Acosta JG, Brownson E, Huang XT, Lopez A, Mendez H, Oliveros S, Vargas JER, Zatserklyaniy A, Alagoz E, Barnes VE, Benedetti D, Bolla G, Bortoletto D, De Mattia M, Everett A, Hu Z, Jones M, Koybasi O, Kress M, Laasanen AT, Leonardo N, Maroussov V, Merkel P, Miller DH, Neumeister N, Shipsey I, Silvers D, Svyatkovskiy A, Marono MV, Yoo HD, Zablocki J, Zheng Y, Guragain S, Parashar N, Adair A, Boulahouache C, Ecklund KM, Geurts FJM, Padley BP, Redjimi R, Roberts J, Zabel J, Betchart B, Bodek A, Chung YS, Covarelli R, de Barbaro P, Demina R, Eshaq Y, Garcia-Bellido A, Goldenzweig P, Han J, Harel A, Miner DC, Vishnevskiy D, Zielinski M, Bhatti A, Ciesielski R, Demortier L, Goulianos K, Lungu G, Malik S, Mesropian C, Arora S, Barker A, Chou JP, Contreras-Campana C, Contreras-Campana E, Duggan D, Ferencek D, Gershtein Y, Gray R, Halkiadakis E, Hidas D, Lath A, Panwalkar S, Park M, Patel R, Rekovic V, Robles J, Rose K, Salur S, Schnetzer S, Seitz C, Somalwar S, Stone R, Thomas S, Cerizza G, Hollingsworth M, Spanier S, Yang ZC, York A, Eusebi R, Flanagan W, Gilmore J, Kamon T, Khotilovich V, Montalvo R, Osipenkov I, Pakhotin Y, Perloff A, Roe J, Safonov A, Sakuma T, Sengupta S, Suarez I, Tatarinov A, Toback D, Akchurin N, Damgov J, Dragoiu C, Dudero PR, Jeong C, Kovitanggoon K, Lee SW, Libeiro T, Roh Y, Volobouev I, Appelt E, Delannoy AG, Florez C, Greene S, Gurrola A, Johns W, Johnston C, Kurt P, Maguire C, Melo A, Sharma M, Sheldon P, Snook B, Tuo S, Velkovska J, Arenton MW, Balazs M, Boutle S, Cox B, Francis B, Goodell J, Hirosky R, Ledovskoy A, Lin C, Neu C, Wood J, Yohay R, Gollapinni S, Harr R, Karchin PE, Don CKK, Lamichhane P, Sakharov A, Anderson M, Belknap D, Borrello L, Carlsmith D, Cepeda M, Dasu S, Friis E, Gray L, Grogg KS, Grothe M, Hall-Wilton R, Herndon M, Herve A, Klabbers P, Klukas J, Lanaro A, Lazaridis C, Leonard J, Loveless R, Mohapatra A, Ojalvo I, Palmonari F, Pierro GA, Ross I, Savin A, Smith WH, Swanson J
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Combined search for the quarks of a sequential fourth generation
PHYSICAL REVIEW D 2012 DEC 12; 86(11):? Article 112003
Results are presented from a search for a fourth generation of quarks produced singly or in pairs in a data set corresponding to an integrated luminosity of 5 fb(-1) recorded by the CMS experiment at the LHC in 2011. A novel strategy has been developed for a combined search for quarks of the up and down type in decay channels with at least one isolated muon or electron. Limits on the mass of the fourth-generation quarks and the relevant Cabibbo-Kobayashi-Maskawa matrix elements are derived in the context of a simple extension of the standard model with a sequential fourth generation of fermions. The existence of mass-degenerate fourth-generation quarks with masses below 685 GeV is excluded at 95% confidence level for minimal off-diagonal mixing between the third- and the fourth-generation quarks. With a mass difference of 25 GeV between the quark masses, the obtained limit on the masses of the fourth-generation quarks shifts by about +/- 20 GeV. These results significantly reduce the allowed parameter space for a fourth generation of fermions. DOI: 10.1103/PhysRevD.86.112003
Aaltonen T, Adelman J, Gonzalez BA, Amerio S, Amidei D, Anastassov A, Annovi A, Antos J, Apollinari G, Appel JA, Arisawa T, Artikov A, Asaadi J, Ashmanskas W, Auerbach B, Aurisano A, Azfar F, Badgett W, Bae T, Barbaro-Galtieri A, Barnes VE, Barnett BA, Barria P, Bartos P, Bauce M, Bedeschi F, Behari S, Bellettini G, Bellinger J, Benjamin D, Beretvas A, Bhatti A, Bisello D, Bizjak I, Bland KR, Blumenfeld B, Bocci A, Bodek A, Bortoletto D, Boudreau J, Boveia A, Brigliadori L, Bromberg C, Brucken E, Budagov J, Budd HS, Burkett K, Busetto G, Bussey P, Buzatu A, Calamba A, Calancha C, Camarda S, Campanelli M, Campbell M, Canelli F, 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, Chen YC, Chertok M, Chiarelli G, Chlachidze G, Chlebana F, Cho K, Chokheli D, Chung WH, Chung YS, Ciocci MA, Clark A, Clarke C, Compostella G, Convery ME, Conway J, Corbo M, Cordelli M, Cox CA, Cox DJ, Crescioli F, Cuevas J, Culbertson R, Dagenhart D, d'Ascenzo N, Datta M, de Barbaro P, Dell'Orso M, Demortier L, Deninno M, Devoto F, d'Errico M, Di Canto A, Di Ruzza B, Dittmann JR, D'Onofrio M, Donati S, Dong P, Dorigo M, Dorigo T, Ebina K, Elagin A, Eppig A, Erbacher R, Errede S, Ershaidat N, Eusebi R, Farrington S, Feindt M, Fernandez JP, Field R, Flanagan G, Forrest R, Frank MJ, Franklin M, Freeman JC, Funakoshi Y, Furic I, Gallinaro M, Garcia JE, Garfinkel AF, Garosi P, Gerberich H, Gerchtein E, Giagu S, Giakoumopoulou V, Giannetti P, Gibson K, Ginsburg CM, Giokaris N, Giromini P, Giurgiu G, Glagolev V, Glenzinski D, Gold M, Goldin D, Goldschmidt N, Golossanov A, Gomez G, Gomez-Ceballos G, Goncharov M, Gonzalez O, Gorelov I, Goshaw AT, Goulianos K, Grinstein S, Grosso-Pilcher C, Group RC, da Costa JG, Hahn SR, Halkiadakis E, Hamaguchi A, Han JY, Happacher F, Hara K, Hare D, Hare M, Harr RF, Hatakeyama K, Hays C, Heck M, Heinrich J, Herndon M, Hewamanage S, Hocker A, Hopkins W, Horn D, Hou S, Hughes RE, Hurwitz M, Husemann U, Hussain N, Hussein M, Huston J, Introzzi G, Iori M, Ivanov A, James E, Jang D, Jayatilaka B, Jeon EJ, Jindariani S, Jones M, Joo KK, Jun SY, Junk TR, Kamon T, Karchin PE, Kasmi A, Kato Y, Ketchum W, Keung J, Khader M, Khotilovich V, Kilminster B, Kim DH, Kim HS, Kim JE, Kim MJ, Kim SB, Kim SH, Kim YK, Kim YJ, Kimura N, Kirby M, Klimenko S, Knoepfel K, Kondo K, Kong DJ, Konigsberg J, Kotwal AV, Kreps M, Kroll J, Krop D, Kruse M, Krutelyov V, Kuhr T, Kurata M, Kwang S, Laasanen AT, Lami S, Lammel S, Lancaster M, Lander RL, Lannon K, Lath A, Latino G, LeCompte T, Lee E, Lee HS, Lee JS, Lee SW, Leo S, Leone S, Lewis JD, Limosani A, Lin CJ, Lindgren M, Lipeles E, Lister A, Litvintsev DO, Liu C, Liu H, Liu Q, Liu T, Lockwitz S, Loginov A, Lucchesi D, Lueck J, Lujan P, Lukens P, Lungu G, Lys J, Lysak R, Madrak R, Maeshima K, Maestro P, Malik S, Manca G, Manousakis-Katsikakis A, Margaroli F, Marino C, Martinez M, Mastrandrea P, Matera K, Mattson ME, Mazzacane A, Mazzanti P, McFarland KS, McIntyre P, McNulty R, Mehta A, Mehtala P, Mesropian C, Miao T, Mietlicki D, Mitra A, Miyake H, Moed S, Moggi N, Mondragon MN, Moon CS, Moore R, Morello MJ, Morlock J, Fernandez PM, Mukherjee A, Muller T, Murat P, Mussini M, Nachtman J, Nagai Y, Naganoma J, Nakano I, Napier A, Nett J, Neu C, Neubauer MS, Nielsen J, Nodulman L, Noh SY, Norniella O, Oakes L, Oh SH, Oh YD, Oksuzian I, Okusawa T, Orava R, Ortolan L, Griso SP, Pagliarone C, Palencia E, Papadimitriou V, Paramonov AA, Patrick J, Pauletta G, Paulini M, Paus C, Pellett DE, Penzo A, Phillips TJ, Piacentino G, Pianori E, Pilot J, Pitts K, Plager C, Pondrom L, Poprocki S, Potamianos K, Prokoshin F, Pranko A, Ptohos F, Punzi G, Rahaman A, Ramakrishnan V, Ranjan N, Rao K, Redondo I, Renton P, Rescigno M, Riddick T, Rimondi F, Ristori L, Robson A, Rodrigo T, Rodriguez T, Rogers E, Rolli S, Roser R, Ruffini F, Ruiz A, Russ J, Rusu V, Safonov A, Sakumoto WK, Sakurai Y, Santi L, Sato K, Saveliev V, Savoy-Navarro A, Schlabach P, Schmidt A, Schmidt EE, Schwarz T, Scodellaro L, Scribano A, Scuri F, Seidel S, Seiya Y, Semenov A, Sforza F, Shalhout SZ, Shears T, Shepard PF, Shimojima M, Shochet M, Shreyber-Tecker I, Simonenko A, Sinervo P, Sliwa K, Smith JR, Snider FD, Soha A, Sorin V, Song H, Squillacioti P, Stancari M, St Denis R, Stelzer B, Stelzer-Chilton O, Stentz D, Strologas J, Strycker GL, Sudo Y, Sukhanov A, Suslov I, Takemasa K, Takeuchi Y, Tang J, Tecchio M, Teng PK, Thom J, Thome J, Thompson GA, Thomson E, Toback D, Tokar S, Tollefson K, Tomura T, Tonelli D, Torre S, Torretta D, Totaro P, Trovato M, Ukegawa F, Uozumi S, Varganov A, Vazquez F, Velev G, Vellidis C, Vidal M, Vila I, Vilar R, Vizan J, Vogel M, Volpi G, Wagner P, Wagner RL, Wakisaka T, Wallny R, Wang SM, Warburton A, Waters D, Wester WC, Whiteson D, Wicklund AB, Wicklund E, Wilbur S, Wick F, Williams HH, Wilson JS, Wilson P, Winer BL, Wittich P, Wolbers S, Wolfe H, Wright T, Wu X, Wu Z, Yamamoto K, Yamato D, Yang T, Yang UK, Yang YC, Yao WM, Yeh GP, Yen M, Yi K, Yoh J, Yorita K, Yoshida T, Yu GB, Yu I, Yu SS, Yun JC, Zanetti A, Zeng Y, Zhou C, Zucchelli S
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Search for a heavy vector boson decaying to two gluons in p(p)over-bar collisions at root s=1.96 TeV
PHYSICAL REVIEW D 2012 DEC 5; 86(11):? Article 112002
We present a search for a new heavy vector boson Z' that decays to gluons. Decays to on-shell gluons are suppressed, leading to a dominant decay mode of Z' -> g*g. We study the case where the off-shell gluon g* converts to a pair of top quarks, leading to a final state of t (t) over barg. In a sample of events with exactly one charged lepton, large missing transverse momentum and at least five jets, corresponding to an integrated luminosity of 8.7 fb(-1) collected by the CDF II detector, we find the data to be consistent with the standard model. We set upper limits on the production cross section times branching ratio of this chromophilic Z' at 95% confidence level from 300 to 40 fb for Z' masses ranging from 400 to 1000 GeV/c(2), respectively.
Brautigam H, Steele JW, Westaway D, Fraser PE, St George-Hyslop PH, Gandy S, Hof PR, Dickstein DL
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The isotropic fractionator provides evidence for differential loss of hippocampal neurons in two mouse models of Alzheimer's disease
MOLECULAR NEURODEGENERATION 2012 NOV 22; 7(?):? Article 58
Background: The accumulation of amyloid beta (A beta) oligomers or fibrils is thought to be one of the main causes of synaptic and neuron loss, believed to underlie cognitive dysfunction in Alzheimer's disease (AD). Neuron loss has rarely been documented in amyloid precursor protein (APP) transgenic mouse models. We investigated whether two APP mouse models characterized by different folding states of amyloid showed different neuronal densities using an accurate method of cell counting. Findings: We examined total cell and neuronal populations in Swedish/Indiana APP mutant mice (TgCRND8) with severe A beta pathology that includes fibrils, plaques, and oligomers, and Dutch APP mutant mice with only A beta oligomer pathology. Using the isotropic fractionator, we found no differences from control mice in regional total cell populations in either TgCRND8 or Dutch mice. However, there were 31.8% fewer hippocampal neurons in TgCRND8 compared to controls, while no such changes were observed in Dutch mice. Conclusions: We show that the isotropic fractionator is a convenient method for estimating neuronal content in milligram quantities of brain tissue and represents a useful tool to assess cell loss efficiently in transgenic models with different types of neuropathology. Our data support the hypothesis that TgCRND8 mice with a spectrum of A beta plaque, fibril, and oligomer pathology exhibit neuronal loss whereas Dutch mice with only oligomers, showed no evidence for neuronal loss. This suggests that the combination of plaques, fibrils, and oligomers causes more damage to mouse hippocampal neurons than A beta oligomers alone.
Zhou Y, Kruyer A, Ho A, Kreek MJ
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Cocaine place conditioning increases pro-opiomelanocortin gene expression in rat hypothalamus
NEUROSCIENCE LETTERS 2012 NOV 14; 530(1):59-63
Recent research suggests an involvement of pro-opiomelanocortin (POMC) gene products in modulating cocaine reward and addiction-like behaviors in rodents. In this study, we investigated whether cocaine-induced conditioned place preference (CPP) alters POMC gene expression in the brain or pituitary of rats. Sprague-Dawley rats were conditioned with 4 injections of 0, 10 or 30 mg/kg cocaine (i.p.) over 8 days and tested 4 days after the last conditioning session. Another group received the same pattern of cocaine injections without conditioning. POMC mRNA levels in the hypothalamus (including arcuate nucleus), amygdala and anterior pituitary, as well as plasma ACTH and corticosterone levels were measured. Cocaine place conditioning at 10 and 30 mg/kg doses increased POMC mRNA levels in a dose-dependent manner in the hypothalamus, with no effect in the amygdala. Cocaine CPP had no effect on POMC mRNA levels in the anterior pituitary or on plasma ACTH or corticosterone levels. In rats that received cocaine at 30 mg/kg without conditioning, there was no such effect on hypothalamic POMC mRNA levels. Alteration of POMC gene expression in the hypothalamus is region-specific after cocaine place conditioning, and dose-dependent. The increased POMC gene expression in the hypothalamus suggests that it is involved in the reward/learning process of cocaine-induced conditioning. (C) 2012 Elsevier Ireland Ltd. All rights reserved.