492 research outputs found

    Tevatron Collider Operations and Plans

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    Run II of the Tevatron Collider is reviewed, emphasizing operations through March 15, 2004. The Run II Luminosity Upgrade plans and luminosity projections through 2009 are discussed.Comment: 8 pages - including 4 figures and 1 photograph to be published in proceedings of XXXIXth Rencontre de Moriond conference on ElectroWeak Interactions and Unified Theories, La Thuile, Aosta Valley, Italy, March 21-28, 200

    Mechanical Regulation of Striated Muscle Nitric Oxide Signaling in Muscular Dystrophy

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    The dystrophin-glycoprotein complex (DGC) is a transmembrane structure that links the cytoskeleton of muscle cells to the extracellular matrix. Genetic disruption of this complex in muscular dystrophies causes sarcolemmal instability that results in injury and death of the muscle cells and causes altered activation of mechanosensitive signaling pathways. These features suggest dual structural and signaling roles for the dystrophin-glycoprotein complex. While much research has focused on protein-protein interactions that enable the DGC’s structural function, less is known about how the complex regulates signaling within muscle cells. Therefore, the goal of this thesis was to investigate the mechanisms whereby the dystrophin-glycoprotein complex regulates muscle nitric oxide (NO) production, a phenomenon that is crucial to normal muscle function and is disrupted in several forms of muscular dystrophy. A novel live cell imaging assay was developed to measure the mechanical activation of NO production in isolated muscle cells and investigate the biochemical signaling pathways involved in this process. This investigation identified dystrophin-dependent mechanoregulation of AMP-activated protein kinase (AMPK) as a key component of mechanosensitive NO production in striated muscle. Since defective muscle NO production contributes to diminished exercise tolerance in muscular dystrophy, subsequent studies investigated the therapeutic potential for acute pharmacologic AMPK activation to restore striated muscle NO production and improve exercise tolerance in a mouse model of dystrophin-deficient muscular dystrophy. Acute AMPK activation stimulated NO production in isolated dystrophin-deficient striated muscle cells in vitro, and increased the exercise capacity of dystrophin-deficient mice in vivo. These results suggest that acute AMPK activation may be a viable therapeutic strategy to improve exercise tolerance in muscular dystrophy patients. Finally, a novel transgenic mouse model was generated in order to test the contribution of asymmetric dimethylarginine (ADMA), an endogenous nitric oxide synthase inhibitor, to poor exercise tolerance in muscular dystrophy. These experiments suggested that ADMA contributes to exercise-induced fatigue in female dystrophin-heterozygous mice, a model for female carriers of Duchenne muscular dystrophy mutations. They also indicated that ADMA may affect exercise tolerance via effects to promote hypertrophy and impair the contractile function of the dystrophin-heterozygous heart. Considered together, the findings of this thesis support the idea that nitric oxide production is impaired in dystrophin-deficient muscle due to combined effects of disrupted intracellular signaling cascades and increased release of endogenous nitric oxide synthase inhibitors from damaged cells. Thus, this research provides evidence for the hypothesis that both the structural and signaling functions of the dystrophin-glycoprotein complex are critical for the appropriate regulation of striated muscle nitric oxide production.PHDMolecular and Integrative PhysiologyUniversity of Michigan, Horace H. Rackham School of Graduate Studieshttps://deepblue.lib.umich.edu/bitstream/2027.42/138767/1/jgarbinc_1.pd

    Recent Tevatron results on heavy ïŹ‚avors

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    CDF presents the ïŹrst measurement of the B± c cross section and D0 presents the observation of a new B0 sπ± state based on the full ∌ 10fb−1 RunII data set at the Fermilab Tevatron 1.96TeV pp collide

    Top quark physics in hadron collisions

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    The top quark is the heaviest elementary particle observed to date. Its large mass makes the top quark an ideal laboratory to test predictions of perturbation theory concerning heavy quark production at hadron colliders. The top quark is also a powerful probe for new phenomena beyond the Standard Model of particle physics. In addition, the top quark mass is a crucial parameter for scrutinizing the Standard Model in electroweak precision tests and for predicting the mass of the yet unobserved Higgs boson. Ten years after the discovery of the top quark at the Fermilab Tevatron top quark physics has entered an era where detailed measurements of top quark properties are undertaken. In this review article an introduction to the phenomenology of top quark production in hadron collisions is given, the lessons learned in Tevatron Run I are summarized, and first Run II results are discussed. A brief outlook to the possibilities of top quark research a the Large Hadron Collider, currently under construction at CERN, is included.Comment: 84 pages, 32 figures, accepted for publication by Reports on Progress in Physic

    Search for CP violation in D0 and D+ decays

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    A high statistics sample of photoproduced charm particles from the FOCUS (E831) experiment at Fermilab has been used to search for CP violation in the Cabibbo suppressed decay modes D+ to K-K+pi+, D0 to K-K+ and D0 to pi-pi+. We have measured the following CP asymmetry parameters: A_CP(K-K+pi+) = +0.006 +/- 0.011 +/- 0.005, A_CP(K-K+) = -0.001 +/- 0.022 +/- 0.015 and A_CP(pi-pi+) = +0.048 +/- 0.039 +/- 0.025 where the first error is statistical and the second error is systematic. These asymmetries are consistent with zero with smaller errors than previous measurements.Comment: 12 pages, 4 figure
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