Elliptic flow in Au+Au collisions at sqrt sNN = 130 GeV

Elliptic flow from nuclear collisions is a hadronic observable sensitive to the early stages of system evolution. We report first results on elliptic flow of charged particles at midrapidity in Au+Au collisions at sqrt[sNN] = 130 GeV using the STAR Time Projection Chamber at the Relativistic Heavy Ion Collider. The elliptic flow signal, v2, averaged over transverse momentum, reaches values of about 6% for relatively peripheral collisions and decreases for the more central collisions. This can be interpreted as the observation of a higher degree of thermalization than at lower collision energies. Pseudorapidity and transverse momentum dependence of elliptic flow are also presented.alle Autoren: K. H. Ackermann19, N. Adams28, C. Adler12, Z. Ahammed27, S. Ahmad28, C. Allgower13, J. Amsbaugh34, M. Anderson6, E. Anderssen17, H. Arnesen3, L. Arnold14, G. S. Averichev10, A. Baldwin16, J. Balewski13, O. Barannikova10,27, L. S. Barnby16, J. Baudot14, M. Beddo1, S. Bekele24, V. V. Belaga10, R. Bellwied35, S. Bennett35, J. Bercovitz17, J. Berger12, W. Betts24, H. Bichsel34, F. Bieser17, L. C. Bland13, M. Bloomer17, C. O. Blyth4, J. Boehm17, B. E. Bonner28, D. Bonnet14, R. Bossingham17, M. Botlo3, A. Boucham30, N. Bouillo30, S. Bouvier30, K. Bradley17, F. P. Brady6, E. S. Braithwaite2, W. Braithwaite2, A. Brandin21, R. L. Brown3, G. Brugalette34, C. Byrd2, H. Caines24, M. Calderón de la Barca Sánchez36, A. Cardenas27, L. Carr34, J. Carroll17, J. Castillo30, B. Caylor17, D. Cebra6, S. Chatopadhyay35, M. L. Chen3, W. Chen3, Y. Chen7, S. P. Chernenko10, M. Cherney9, A. Chikanian36, B. Choi31, J. Chrin9, W. Christie3, J. P. Coffin14, L. Conin30, C. Consiglio3, T. M. Cormier35, J. G. Cramer34, H. J. Crawford5, V. I. Danilov10, D. Dayton3, M. DeMello28, W. S. Deng16, A. A. Derevschikov26, M. Dialinas30, H. Diaz3, P. A. DeYoung8, L. Didenko3, D. Dimassimo3, J. Dioguardi3, W. Dominik32, C. Drancourt30, J. E. Draper6, V. B. Dunin10, J. C. Dunlop36, V. Eckardt19, W. R. Edwards17, L. G. Efimov10, T. Eggert19, V. Emelianov21, J. Engelage5, G. Eppley28, B. Erazmus30, A. Etkin3, P. Fachini29, C. Feliciano3, D. Ferenc6, M. I. Ferguson7, H. Fessler19, E. Finch36, V. Fine3, Y. Fisyak3, D. Flierl12, I. Flores5, K. J. Foley3, D. Fritz17, N. Gagunashvili10, J. Gans36, M. Gazdzicki12, M. Germain14, F. Geurts28, V. Ghazikhanian7, C. Gojak14, J. Grabski33, O. Grachov35, M. Grau3, D. Greiner17, L. Greiner5, V. Grigoriev21, D. Grosnick1, J. Gross9, G. Guilloux30, E. Gushin21, J. Hall35, T. J. Hallman3, D. Hardtke17, G. Harper34, J. W. Harris36, P. He5, M. Heffner6, S. Heppelmann25, T. Herston27, D. Hill1, B. Hippolyte14, A. Hirsch27, E. Hjort27, G. W. Hoffmann31, M. Horsley36, M. Howe34, H. Z. Huang7, T. J. Humanic24, H. Hümmler19, W. Hunt13, J. Hunter17, G. J. Igo7, A. Ishihara31, Yu. I. Ivanshin11, P. Jacobs17, W. W. Jacobs13, S. Jacobson17, R. Jared17, P. Jensen31, I. Johnson17, P. G. Jones4, E. Judd5, M. Kaneta17, M. Kaplan8, D. Keane16, V. P. Kenney23*, A. Khodinov21, J. Klay6, S. R. Klein17, A. Klyachko13, G. Koehler17, A. S. Konstantinov26, V. Kormilitsyne7,26, L. Kotchenda21, I. Kotov24, A. D. Kovalenko10, M. Kramer22, P. Kravtsov21, K. Krueger1, T. Krupien3, P. Kuczewski3, C. Kuhn14, G. J. Kunde36, C. L. Kunz8, R. Kh. Kutuev11, A. A. Kuznetsov10, L. Lakehal-Ayat30, J. Lamas-Valverde28, M. A. C. Lamont4, J. M. Landgraf3, S. Lange12, C. P. Lansdell31, B. Lasiuk36, F. Laue24, A. Lebedev3, T. LeCompte1, W. J. Leonhardt3, V. M. Leontiev26, P. Leszczynski33, M. J. LeVine3, Q. Li35, Q. Li17, Z. Li3, C.-J. Liaw3, J. Lin9, S. J. Lindenbaum22, V. Lindenstruth5, P. J. Lindstrom5, M. A. Lisa24, H. Liu16, T. Ljubicic3, W. J. Llope28, G. LoCurto19, H. Long7, R. S. Longacre3, M. Lopez-Noriega24, D. Lopiano1, W. A. Love3, J. R. Lutz14, D. Lynn3, L. Madansky15§, R. Maier19, R. Majka36, A. Maliszewski33, S. Margetis16, K. Marks17, R. Marstaller19, L. Martin30, J. Marx17, H. S. Matis17, Yu. A. Matulenko26, E. A. Matyushevski10, C. McParland17, T. S. McShane9, J. Meier9, Yu. Melnick26, A. Meschanin26, P. Middlekamp3, N. Mikhalin7,26, B. Miller3, Z. Milosevich8, N. G. Minaev26, B. Minor17, J. Mitchell15, E. Mogavero3, V. A. Moiseenko11, D. Moltz17, C. F. Moore31, V. Morozov17, R. Morse17, M. M. de Moura29, M. G. Munhoz29, G. S. Mutchler28, J. M. Nelson4, P. Nevski3, T. Ngo7, M. Nguyen3, T. Nguyen3, V. A. Nikitin11, L. V. Nogach26, T. Noggle17, B. Norman16, S. B. Nurushev26, T. Nussbaum28, J. Nystrand17, G. Odyniec17, A. Ogawa25, C. A. Ogilvie18, K. Olchanski3, M. Oldenburg19, D. Olson17, G. A. Ososkov10, G. Ott31, D. Padrazo3, G. Paic24, S. U. Pandey35, Y. Panebratsev10, S. Y. Panitkin16, A. I. Pavlinov26, T. Pawlak33, M. Pentia10, V. Perevotchikov3, W. Peryt33, V. A Petrov11, W. Pinganaud30, S. Pirogov7, E. Platner28, J. Pluta33, I. Polk3, N. Porile27, J. Porter3, A. M. Poskanzer17, E. Potrebenikova10, D. Prindle34, C. Pruneau35, J. Puskar-Pasewicz13, G. Rai17, J. Rasson17, O. Ravel30, R. L. Ray31, S. V. Razin10,13, D. Reichhold9, J. Reid34, R. E. Renfordt12, F. Retiere30, A. Ridiger21, J. Riso35, H. G. Ritter17, J. B. Roberts28, D. Roehrich12, O. V. Rogachevski10, J. L. Romero6, C. Roy30, D. Russ8, V. Rykov35, I. Sakrejda17, R. Sanchez7, Z. Sandler7, J. Sandweiss36, P. Sappenfield28, A. C. Saulys3, I. Savin11, J. Schambach31, R. P. Scharenberg27, J. Scheblien3, R. Scheetz3, R. Schlueter17, N. Schmitz19, L. S. Schroeder17, M. Schulz3,19, A. Schüttauf19, J. Sedlmeir3, J. Seger9, D. Seliverstov21, J. Seyboth19, P. Seyboth19, R. Seymour34, E. I. Shakaliev10, K. E. Shestermanov26, Y. Shi7, S. S. Shimanskii10, D. Shuman17, V. S. Shvetcov11, G. Skoro10, N. Smirnov36, L. P. Smykov10, R. Snellings17, K. Solberg13, J. Sowinski13, H. M. Spinka1, B. Srivastava27, E. J. Stephenson13, R. Stock12, A. Stolpovsky35, N. Stone3, R. Stone17, M. Strikhanov21, B. Stringfellow27, H. Stroebele12, C. Struck12, A. A. P. Suaide29, E. Sugarbaker24, C. Suire14, T. J. M. Symons17, J. Takahashi29, A. H. Tang16, A. Tarchini14, J. Tarzian17, J. H. Thomas17, V. Tikhomirov21, A. Szanto de Toledo29, S. Tonse17, T. Trainor34, S. Trentalange7, M. Tokarev10, M. B. Tonjes20, V. Trofimov21, O. Tsai7, K. Turner3, T. Ullrich36, D. G. Underwood1, I. Vakula7, G. Van Buren3, A. M. VanderMolen20, A. Vanyashin17, I. M. Vasilevski11, A. N. Vasiliev26, S. E. Vigdor13, G. Visser5, S. A. Voloshin35, C. Vu17, F. Wang27, H. Ward31, D. Weerasundara34, R. Weidenbach17, R. Wells17, R. Wells24, T. Wenaus3, G. D. Westfall20, J. P. Whitfield8, C. Whitten, Jr.7, H. Wieman17, R. Willson24, K. Wilson35, J. Wirth17, J. Wisdom7, S. W. Wissink13, R. Witt16, J. Wolf17, L. Wood6, N. Xu17, Z. Xu36, A. E. Yakutin26, E. Yamamoto7, J. Yang7, P. Yepes28, A. Yokosawa1, V. I. Yurevich10, Y. V. Zanevski10, J. Zhang17, W. M. Zhang16, J. Zhu34, D. Zimmerman17, R. Zoulkarneev11, and A. N. Zubare

Molecular mechanisms of inflammation and tissue injury after major trauma-is complement the "bad guy"?

Trauma represents the leading cause of death among young people in industrialized countries. Recent clinical and experimental studies have brought increasing evidence for activation of the innate immune system in contributing to the pathogenesis of trauma-induced sequelae and adverse outcome. As the "first line of defense", the complement system represents a potent effector arm of innate immunity, and has been implicated in mediating the early posttraumatic inflammatory response. Despite its generic beneficial functions, including pathogen elimination and immediate response to danger signals, complement activation may exert detrimental effects after trauma, in terms of mounting an "innocent bystander" attack on host tissue. Posttraumatic ischemia/reperfusion injuries represent the classic entity of complement-mediated tissue damage, adding to the "antigenic load" by exacerbation of local and systemic inflammation and release of toxic mediators. These pathophysiological sequelae have been shown to sustain the systemic inflammatory response syndrome after major trauma, and can ultimately contribute to remote organ injury and death. Numerous experimental models have been designed in recent years with the aim of mimicking the inflammatory reaction after trauma and to allow the testing of new pharmacological approaches, including the emergent concept of site-targeted complement inhibition. The present review provides an overview on the current understanding of the cellular and molecular mechanisms of complement activation after major trauma, with an emphasis of emerging therapeutic concepts which may provide the rationale for a "bench-to-bedside" approach in the design of future pharmacological strategies

Stability analysis of a class of two-dimensional multipolar vortex equilibria

Published versio

Star Architecture as Socio-Material Assemblage

Taking inspiration from new materialism and assemblage, the chapter deals with star architects and iconic buildings as socio-material network effects that do not pre-exist action, but are enacted in practice, in the materiality of design crafting and city building. Star architects are here conceptualized as part of broader assemblages of actors and practices ‘making star architecture’ a reality, and the buildings they design are considered not just as unique and iconic objects, but dis-articulated as complex crafts mobilizing skills, technologies, materials, and forms of knowledge not necessarily ascribable to architecture. Overcoming narrow criticism focusing on the symbolic order of icons as unique creations and alienated repetitions of capitalist development, the chapter’s main aim is to widen the scope of critique by bridging culture and economy, symbolism and practicality, making star architecture available to a broad, fragmented arena of (potential) critics, unevenly equipped with critical tools and differentiated experiences

2022 Top Trends in Academic Libraries

This article summarizes trending topics in academic librarianship from the past two years–a time of tremendous upheaval and change, including a global pandemic, difficult reflections concerning racial justice, and war between nation states. Rapid changes and uncertainty from these events have created a significant amount of shifts to academic libraries, higher education, and society in general. Such shifts have yielded new perspectives and innovations in how librarians approach delivering services, supporting student success, managing staff and physical spaces, embracing new technology, and managing data. This report attempts to provide a snapshot of developments worth noting

Inclusive production of charged pions in p+C collisions at 158 GeV/c beam momentum

The production of charged pions in minimum bias p+C interactions is studied using a sample of 377000 inelastic events obtained with the NA49 detector at the CERN SPS at 158 GeV/c beam momentum. The data cover a phase space area ranging from 0 to 1.8 GeV/c in transverse momentum and from -0.1 to 0.5 in Feynman x. Inclusive invariant cross sections are given on a grid of 270 bins per charge thus offering for the first time a dense coverage of the projectile hemisphere and of the cross-over region into the target fragmentation zone.Comment: 31 pages, 30 figures, submitted to European Journal of Physic

Adeno-associated virus-mediated gene transfer of the heart/muscle adenine nucleotide translocator (ANT) in mouse

Mitochondrial myopathy, associated with muscle weakness and progressive external ophthalmoplegia, is caused by mutations in mitochondria oxidative phosphorylation genes including the heart–muscle isoform of the mitochondrial adenine nucleotide translocator (ANT1). To develop therapies for mitochondrial disease, we have prepared a recombinant adeno-associated viral vector (rAAV) carrying the mouse Ant1 cDNA. This vector has been used to transduce muscle cells and muscle from Ant1 mutant mice, which manifest mitochondrial myopathy. AAV-ANT1 transduction resulted in long-term, stable expression of the Ant1 transgene in muscle precursor cells as well as differentiated muscle fibers. The transgene ANT1 protein was targeted to the mitochondrion, was inserted into the mitochondrial inner membrane, formed a functional ADP/ATP carrier, increased the mitochondrial export of ATP and reversed the histopathological changes associated with the mitochondrial myopathy. Thus, AAV transduction has the potential of providing symptomatic relief for the ophthalmoplegia and ptosis resulting from paralysis of the extraocular eye muscles cause by mutations in the Ant1 gene

Resonances and fluctuations of strange particle in 200 GeV Au-Au collisions

We perform an analysis of preliminary data on strange particles yields and fluctuations within the Statistical hadronization model. We begin by describing the theoretical disagreements between different statistical models currently on the market. We then show how the simultaneous analysis of yields and fluctuations can be used to differentiate between the different models, and determine if one of them can be connected to underlying physics. We perform a study on a RHIC 200 GeV data sample that includes stable particles, resonances, and the event-by-event fluctuation of the $K/\pi$ ratio. We show that the equilibrium statistical model can not describe the fluctuation, unless an unrealistically small volume is assumed. Such small volume then makes it impossible to describe the total particle multiplicity. The non-equilibrium model,on the other hand, describes both the $K/\pi$ fluctuation and yields acceptably due to the extra boost to the $\pi$ fluctuation provided by the high pion chemical potential. $\Lambda(1520)$ and $K^*$ abundance is described within error bars, but the $\Sigma^*$ is under-predicted to $\sim$ 1.5 standard deviations. We suggest further measurements that have the potential to test the non-equilibrium model, as well as gauge the effect of re-interactions between hadronization and freeze-out.Comment: References added, equations corrected. As accepted for publication by Journal of Physics