Local field effects on the radiative lifetimes of Ce3+^{3+} 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 $4f\to 4f$ radiative transition of Eu$^{3+}$ 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 $5d\to 4f$ 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 $5d\to 4f$ transition of Ce$^{3+}$ 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 K−K^-+pp+pp threshold in the in-flight 3^3He(K−,Λp)n(K^-,\Lambda p)n reaction

To search for an S= -1 di-baryonic state which decays to $\Lambda p$, the ${\rm{}^3He}(K^-,\Lambda p)n_{missing}$ reaction was studied at 1.0 GeV/$c$. Unobserved neutrons were kinematically identified from the missing mass $M_X$ of the ${\rm{}^3He}(K^-,\Lambda p)X$ reaction in order to have a large acceptance for the $\Lambda pn$ final state. The observed $\Lambda p n$ 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 $\Lambda p$. 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 $\chi^2$ method was applied to deduce its mass $M_X\ =$ 2355 $^{+ 6}_{ - 8}$ (stat.) $\pm 12$ (syst.) MeV/c$^2$, and decay-width $\Gamma_X\ =$ 110 $^{+ 19}_{ - 17}$ (stat.) $\pm 27$ (syst.) MeV/c$^2$, respectively. The form factor parameter $Q_X \sim$ 400 MeV/$c$ implies that the range of interaction is about 0.5Comment: 12pages, 8 figure

Search for the decay KL0→3γK_L^0 \rightarrow 3\gamma

We performed a search for the decay $K_L^0 \rightarrow 3\gamma$ 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 $K_L^0 \rightarrow 3\gamma$ proceeding via parity-violation, we obtained the single event sensitivity to be $(3.23\pm0.14)\times10^{-8}$, and set an upper limit on the branching ratio to be $7.4\times10^{-8}$ at the 90% confidence level. This is a factor of 3.2 improvement compared to the previous results. The results of $K_L^0 \rightarrow 3\gamma$ proceeding via parity-conservation were also presented in this paper

Experimental study of the decay KL0→π0ννˉK_L^0\to\pi^0\nu\bar{\nu}

The first dedicated search for the rare neutral-kaon decay $K_L^0\to\pi^0\nu\bar{\nu}$ has been carried out in the E391a experiment at the KEK 12-GeV proton synchrotron. The final upper limit of 2.6 $\times 10^{-8}$ 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