230 research outputs found
Local field effects on the radiative lifetimes of Ce in different hosts
For emitters embedded in media of various refractive indices, different
theoretical models predicted substantially different dependencies of the
spontaneous emission lifetime on refractive index. It has been claimed that
various measurements on radiative transition of Eu in hosts
with variable refractive index appear to favor the real-cavity model [J.
Fluoresc. 13, 201 (2003) and references therein, Phys. Rev. Lett. 91, 203903
(2003)]. We notice that radiative transition of rare-earth ions,
dominated by allowed electric-dipole transitions with line strengths less
perturbed by the ligands, serves as a better test of different models. We
analyze the lifetimes of transition of Ce in hosts of
refractive indices varying from 1.4 to 2.2. The results favor the macroscopic
virtual-cavity model based on Lorentz local field [J. Fluoresc. 13, 201
(2003)].Comment: 9pages, 1 figures, presented on AMN-2 and to appear on Current
Applied Physic
Measurement of the strong interaction induced shift and width of the 1s state of kaonic deuterium at J-PARC
The antikaon-nucleon interaction close to threshold provides crucial
information on the interplay between spontaneous and explicit chiral symmetry
breaking in low-energy QCD. In this context the importance of kaonic deuterium
X-ray spectroscopy has been well recognized, but no experimental results have
yet been obtained due to the difficulty of the measurement. We propose to
measure the shift and width of the kaonic deuterium 1s state with an accuracy
of 60 eV and 140 eV respectively at J-PARC. These results together with the
kaonic hydrogen data (KpX at KEK, DEAR and SIDDHARTA at DAFNE) will then permit
the determination of values of both the isospin I=0 and I=1 antikaon-nucleon
scattering lengths and will provide the most stringent constraints on the
antikaon-nucleon interaction, promising a breakthrough. Refined Monte Carlo
studies were performed, including the investigation of background suppression
factors for the described setup. These studies have demonstrated the
feasibility of determining the shift and width of the kaonic deuterium atom 1s
state with the desired accuracy of 60 eV and 140 eV.Comment: 12 pages, 9 figure
Structure near ++ threshold in the in-flight He reaction
To search for an S= -1 di-baryonic state which decays to , the reaction was studied at 1.0 GeV/.
Unobserved neutrons were kinematically identified from the missing mass
of the reaction in order to have a large
acceptance for the final state. The observed events,
distributed widely over the kinematically allowed region of the Dalitz plot,
establish that the major component comes from a three nucleon absorption
process. A concentration of events at a specific neutron kinetic energy was
observed in a region of low momentum transfer to the . To account
for the observed peak structure, the simplest S-wave pole was assumed to exist
in the reaction channel, having Breit-Wigner form in energy and with a Gaussian
form-factor. A minimum method was applied to deduce its mass
2355 (stat.) (syst.) MeV/c, and decay-width
110 (stat.) (syst.) MeV/c,
respectively. The form factor parameter 400 MeV/ implies that the
range of interaction is about 0.5Comment: 12pages, 8 figure
Search for the decay
We performed a search for the decay with the
E391a detector at KEK. In the data accumulated in 2005, no event was observed
in the signal region. Based on the assumption of
proceeding via parity-violation, we obtained the single event sensitivity to be
, and set an upper limit on the branching ratio to
be at the 90% confidence level. This is a factor of 3.2
improvement compared to the previous results. The results of proceeding via parity-conservation were also presented in this paper
Experimental study of the decay
The first dedicated search for the rare neutral-kaon decay
has been carried out in the E391a experiment at the
KEK 12-GeV proton synchrotron. The final upper limit of 2.6 at
the 90% confidence level was set on the branching ratio for the decay.Comment: 23 pages, 27 figures, accepted for publication as a regular article
in Physical Review
Caveolin-1 protects B6129 mice against Helicobacter pylori gastritis.
Caveolin-1 (Cav1) is a scaffold protein and pathogen receptor in the mucosa of the gastrointestinal tract. Chronic infection of gastric epithelial cells by Helicobacter pylori (H. pylori) is a major risk factor for human gastric cancer (GC) where Cav1 is frequently down-regulated. However, the function of Cav1 in H. pylori infection and pathogenesis of GC remained unknown. We show here that Cav1-deficient mice, infected for 11 months with the CagA-delivery deficient H. pylori strain SS1, developed more severe gastritis and tissue damage, including loss of parietal cells and foveolar hyperplasia, and displayed lower colonisation of the gastric mucosa than wild-type B6129 littermates. Cav1-null mice showed enhanced infiltration of macrophages and B-cells and secretion of chemokines (RANTES) but had reduced levels of CD25+ regulatory T-cells. Cav1-deficient human GC cells (AGS), infected with the CagA-delivery proficient H. pylori strain G27, were more sensitive to CagA-related cytoskeletal stress morphologies ("humming bird") compared to AGS cells stably transfected with Cav1 (AGS/Cav1). Infection of AGS/Cav1 cells triggered the recruitment of p120 RhoGTPase-activating protein/deleted in liver cancer-1 (p120RhoGAP/DLC1) to Cav1 and counteracted CagA-induced cytoskeletal rearrangements. In human GC cell lines (MKN45, N87) and mouse stomach tissue, H. pylori down-regulated endogenous expression of Cav1 independently of CagA. Mechanistically, H. pylori activated sterol-responsive element-binding protein-1 (SREBP1) to repress transcription of the human Cav1 gene from sterol-responsive elements (SREs) in the proximal Cav1 promoter. These data suggested a protective role of Cav1 against H. pylori-induced inflammation and tissue damage. We propose that H. pylori exploits down-regulation of Cav1 to subvert the host's immune response and to promote signalling of its virulence factors in host cells
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