48 research outputs found
A Study of the \eta \pi^{0} Spectrum and Search for a J^{PC} = 1^{-+} Exotic Meson
A partial wave analysis (PWA) of the of the system (where ) produced in the charge exchange reaction at an incident momentum of 18 GeV is presented as a function of
invariant mass, , and momentum transfer squared,
, from the incident to the outgoing system. , and waves were included in the PWA. The
and states are clearly observed in the overall
effective mass distribution as well as in the amplitudes associated with
wave and waves respectively after partial wave decomposition. The observed
distributions in moments (averages of spherical harmonics) were compared to the
results from the PWA and the two are consistent. The distribution in
for individual waves associated with natural and
unnatural parity exchange in the -channel are consistent with Regge
phenomenology. Of particular interest in this study is the wave since this
leads to an exotic for the system. A wave is
present in the data, however attempts to describe the mass dependence of the
amplitude and phase motion with respect to the wave as a Breit-Wigner
resonance are problematic. This has implications regarding the existence of a
reported exotic meson decaying into with a mass
near 1.4 GeV.Comment: 19 pages, 29 figures, to appear in Phys. Rev.
Decay of heavy-light hybrids in HQET sum rules
The decay widths of the 0^{++} and 1^{-+} heavy-light hybrids to B(D) and
pion are calculated by using the QCD sum rules. The interpolated current of the
hybrid is chosen as . In
order to simplify the calculation and avoid the ambiguity of three-point
correlation function, a two-point correlation function between the pion and
vacuum is used instead. The decay width of the is about 12(16)
MeV while the is around 0.4(1.8) MeV. We keep the leading
order of 1/M_Q expansion in our calculation for convenience.Comment: 14 pages, latex file, 4 ps figs, Published version, some numerical
results change
Can the Mechanism for Hybrid Decays be Detected?
Two mechanisms for the () hybrid meson decay processes
are investigated. These mechanisms are applied to
and decays to
illustrate the validity of the decay mechanisms and to obtain independent
information on the coupling of to quark and gluonic operators.
From this information, we find that
is substantially different
in the two decay mechanisms, and hence future experimental measurements of this
ratio will provide valuable information for substantiating the hybrid nature of
these states and for determining the mechanism for these hybrid decays.Comment: 5 pages, revtex, 1 eps figure embedded in manuscript. Analysis and
references extended in v
Evidence for Exotic J^{PC}=1^{-+} Meson Production in the Reaction pi- p --> eta pi- p at 18 GeV/c
Details of the analysis of the eta pi- system studied in the reaction pi^{-}
p --> eta pi^{-} p at 18 GeV/c are given. Separate analyses for the 2 gamma and
pi+ pi- pi0 decay modes of the eta are presented. An amplitude analysis of the
data indicates the presence of interference between the a(2)(1320)- and a
J^{PC}=1^{-+} wave between 1.2 and 1.6 GeV/c^2. The phase difference between
these waves shows phase motion not attributable solely to the a(2)(1320)-. The
data can be fitted by interference between the a(2)(1320)- and an exotic 1^{-+}
resonance with M = 1370 +-16 +50 -30} MeV/c^2 and Gamma = 385 +- 40 +65 -105
MeV/c^2. Our results are compared with those of other experiments.Comment: 50 pages of text and 34 figure
Interpretation of Experimental J^PC Exotic Signals
We investigate theoretical interpretations of the 1.4 GeV J^PC exotic
resonance reported by the E852 collaboration. It is argued that interpretation
in terms of a hybrid meson is untenable. A K-matrix analysis shows that the 1.4
GeV enhancement in the E852 eta pi data can be understood as an interference of
a non-resonant Deck-type background and a resonance at 1.6 GeV. A final state
rescattering calculation shows that the 1.6 GeV hybrid has a eta pi width which
is bounded above by 57 \pm 14 MeV.Comment: 23 pages, LaTeX, 4 encapsulated postscript figures. Accepted for
publication by Physical Review
Regulation of the Fruit-Specific PEP Carboxylase SlPPC2 Promoter at Early Stages of Tomato Fruit Development
The SlPPC2 phosphoenolpyruvate carboxylase (PEPC; EC 4.1.1.31) gene from tomato (Solanum lycopersicum) is differentially and specifically expressed in expanding tissues of developing tomato fruit. We recently showed that a 1966 bp DNA fragment located upstream of the ATG codon of the SlPPC2 gene (GenBank AJ313434) confers appropriate fruit-specificity in transgenic tomato. In this study, we further investigated the regulation of the SlPPC2 promoter gene by analysing the SlPPC2 cis-regulating region fused to either the firefly luciferase (LUC) or the β-glucuronidase (GUS) reporter gene, using stable genetic transformation and biolistic transient expression assays in the fruit. Biolistic analyses of 5′ SlPPC2 promoter deletions fused to LUC in fruits at the 8th day after anthesis revealed that positive regulatory regions are mostly located in the distal region of the promoter. In addition, a 5′ UTR leader intron present in the 1966 bp fragment contributes to the proper temporal regulation of LUC activity during fruit development. Interestingly, the SlPPC2 promoter responds to hormones (ethylene) and metabolites (sugars) regulating fruit growth and metabolism. When tested by transient expression assays, the chimeric promoter:LUC fusion constructs allowed gene expression in both fruit and leaf, suggesting that integration into the chromatin is required for fruit-specificity. These results clearly demonstrate that SlPPC2 gene is under tight transcriptional regulation in the developing fruit and that its promoter can be employed to drive transgene expression specifically during the cell expansion stage of tomato fruit. Taken together, the SlPPC2 promoter offers great potential as a candidate for driving transgene expression specifically in developing tomato fruit from various tomato cultivars
Nucleoside analogs induce proteasomal down-regulation of p21 in chronic lymphocytic leukemia cell lines
Can Communicating Personalised Disease Risk Promote Healthy Behaviour Change? A Systematic Review of Systematic Reviews.
: The assessment and communication of disease risk that is personalised to the individual is widespread in healthcare contexts. Despite several systematic reviews of RCTs, it is unclear under what circumstances that personalised risk estimates promotes change in four key health-related behaviours: smoking, physical activity, diet and alcohol consumption.
: The present research aims to systematically identify, evaluate and synthesise the findings of existing systematic reviews.
: This systematic review of systematic reviews followed published guidance. A search of four databases and two-stage screening procedure with good reliability identified nine eligible systematic reviews.
: The nine reviews each included between three and 15 primary studies, containing 36 unique studies. Methods of personalising risk feedback included imaging/visual feedback, genetic testing, and numerical estimation from risk algorithms. The reviews were generally high quality. For a broad range of methods of estimating and communicating risk, the reviews found no evidence that risk information had strong or consistent effects on health-related behaviours. The most promising effects came from interventions using visual or imaging techniques and with smoking cessation and dietary behaviour as outcomes, but with inconsistent results. Few interventions explicitly used theory, few targeted self-efficacy or response efficacy, and a limited range of Behaviour Change Techniques were used.
: Presenting risk information on its own, even when highly personalised, does not produce strong effects on health-related behaviours or changes which are sustained. Future research in this area should build on the existing knowledge base about increasing the effects of risk communication on behaviour.The present research was funded partly by Research Capability Funding from NIHR CLAHRC Greater Manchester and the charity Prevent Breast Cancer