CP Violation Studies at Tevatron

We present an overview of a few recent results related to CP-violation from the Tevatron. First, we discuss a measurement of the dimuon charge asymmetry from D{\O}that extracts the CP-violation parameter of \Bo mixing and decay. This is followed by the CDF measurement of the CP-violating asymmetry in \bdkpi decays. Finally we give the CDF result on the ratio $R = \frac{BR(B \to D^0 K)}{BR(B \to D^0 \pi)}$Comment: 4 pages. Talk given at BEACH 2006, Lancaster, Englan

Evolution of constrained layer damping using a cellular automaton algorithm

Constrained layer damping (CLD) is a highly effective passive vibration control strategy if optimized adequately. Factors controlling CLD performance are well documented for the flexural modes of beams but not for more complicated mode shapes or structures. The current paper introduces an approach that is suitable for locating CLD on any type of structure. It follows the cellular automaton (CA) principle and relies on the use of finite element models to describe the vibration properties of the structure. The ability of the algorithm to reach the best solution is demonstrated by applying it to the bending and torsion modes of a plate. Configurations that give the most weight-efficient coverage for each type of mode are first obtained by adapting the existing 'optimum length' principle used for treated beams. Next, a CA algorithm is developed, which grows CLD patches one at a time on the surface of the plate according to a simple set of rules. The effectiveness of the algorithm is then assessed by comparing the generated configurations with the known optimum ones

<i>Vibrio coralliilyticus</i> sp. nov., a temperature-dependent pathogen of the coral <i>Pocillopora damicornis</i>

Vibrio sp. YB1T (=ATCC BAA-450T =LMG 20984T), the aetiological agent of tissue lysis of the coral Pocillopora damicornis, was characterized as a novel Vibrio species on the basis of 16S rDNA sequence, DNA-DNA hybridization data (G+C content is 45·6 mol%), AFLP and GTG5-PCR genomic fingerprinting patterns and phenotypic properties, including the cellular fatty acid profile. The predominant fatty acids were 16 : 0 and 18 : 1?7c. The name Vibrio coralliilyticus sp. nov. is proposed for the novel coral-pathogenic species. In addition to strain YB1T, which was isolated from the Indian Ocean, five additional strains of V. coralliilyticus have been isolated, three from diseased P. damicornis in the Red Sea, one from diseased oyster larvae (Kent, UK) and one from bivalve larvae (Brazil). The six V. coralliilyticus strains showed high genotypic and phenotypic similarities and all were pathogenic to P. damicornis. The closest phylogenetic neighbours to V. coralliilyticus are Vibrio tubiashii, Vibrio nereis and Vibrio shilonii</i

Extraction of the x-dependence of the non-perturbative QCD b-quark fragmentation distribution component

Using recent measurements of the b-quark fragmentation distribution obtained in $e^+e^- \to b \bar{b}$ events registered at the Z pole, the non-perturbative QCD component of the distribution has been extracted independently of any hadronic physics modelling. This distribution depends only on the way the perturbative QCD component has been defined. When the perturbative QCD component is taken from a parton shower Monte-Carlo, the non-perturbative QCD component is rather similar with those obtained from the Lund or Bowler models. When the perturbative QCD component is the result of an analytic NLL computation, the non-perturbative QCD component has to be extended in a non-physical region and thus cannot be described by any hadronic modelling. In the two examples used to characterize these two situations, which are studied at present, it happens that the extracted non-perturbative QCD distribution has the same shape, being simply translated to higher-x values in the second approach, illustrating the ability of the analytic perturbative QCD approach to account for softer gluon radiation than with a parton shower generator.Comment: 13 page

Quantitative SPECT/CT parameters of myocardial 99mTechnetium-3,3-diphosphono-1,2-propanodicarboxylic acid (DPD) uptake in suspected cardiac transthyretin amyloidosis

Background: 99mTc-labelled bisphosphonates are used for imaging assessment of patients with transthyretin cardiac amyloidosis (ATTR). Present study evaluates whether quantitative SPECT/CT measurement of absolute myocardial 99mTc-labelled 3,3-diphosphono-1,2-propanodicarboxylic acid (Tc-DPD) uptake can diagnose patients with suspected ATTR. / Methods: Twenty-eight patients (25 male, age 80.03 ± 6.99 years) with suspected ATTR referred for Tc-DPD imaging had planar and SPECT/CT imaging of the chest. Three operators independently obtained Tc-DPD myocardial SUVmax and SUVmean above threshold (SMaT) (20, 40 and 60% of SUVmax), using a semi-automated threshold segmentation method. Results were compared to visual grading (0–3) of cardiac uptake. / Results: Twenty-two patients (78%) had cardiac uptake (2 grade 1, 15 grade 2, 5 grade 3). SUVmax and SMaT segmentation thresholds enabled separating grades 2/3 from 0/1 with excellent inter- and intra-reader correlation. Cut-off values 6.0, 2.5, 3 and 4 for SUVmax, SMaT20,40,60, respectively, separated between grades 2/3 and 0 /1 with PPV and NPV of 100%. SMaT20,40,60(cardiac)/SUVmean (liver) and SMaT20,40,60(cardiac)/SUVmean(liver/lung) separated grades 2 and 3. / Conclusion: Quantitative SPECT/CT parameters of cardiac Tc-DPD uptake are robust, enabling separation of patients with grades 2 and 3 cardiac uptake from grades 0 and 1. Larger patient cohorts will determine the incremental value of SPECT/CT quantification for ATTR management

The JAK/STAT3 Pathway Is a Common Inducer of Astrocyte Reactivity in Alzheimer's and Huntington's Diseases.

Astrocyte reactivity is a hallmark of neurodegenerative diseases (ND), but its effects on disease outcomes remain highly debated. Elucidation of the signaling cascades inducing reactivity in astrocytes during ND would help characterize the function of these cells and identify novel molecular targets to modulate disease progression. The Janus kinase/signal transducer and activator of transcription 3 (JAK/STAT3) pathway is associated with reactive astrocytes in models of acute injury, but it is unknown whether this pathway is directly responsible for astrocyte reactivity in progressive pathological conditions such as ND. In this study, we examined whether the JAK/STAT3 pathway promotes astrocyte reactivity in several animal models of ND. The JAK/STAT3 pathway was activated in reactive astrocytes in two transgenic mouse models of Alzheimer's disease and in a mouse and a nonhuman primate lentiviral vector-based model of Huntington's disease (HD). To determine whether this cascade was instrumental for astrocyte reactivity, we used a lentiviral vector that specifically targets astrocytes in vivo to overexpress the endogenous inhibitor of the JAK/STAT3 pathway [suppressor of cytokine signaling 3 (SOCS3)]. SOCS3 significantly inhibited this pathway in astrocytes, prevented astrocyte reactivity, and decreased microglial activation in models of both diseases. Inhibition of the JAK/STAT3 pathway within reactive astrocytes also increased the number of huntingtin aggregates, a neuropathological hallmark of HD, but did not influence neuronal death. Our data demonstrate that the JAK/STAT3 pathway is a common mediator of astrocyte reactivity that is highly conserved between disease states, species, and brain regions. This universal signaling cascade represents a potent target to study the role of reactive astrocytes in ND

Unexpected expression of carbonic anhydrase I and selenium‐binding protein as the only major non‐heme proteins in erythrocytes of the subterranean mole rat (Spalax ehrenbergi)

Peer Reviewedhttp://deepblue.lib.umich.edu/bitstream/2027.42/117190/1/feb2s0014579398006905.pd