Pygmy Dipol Resonances as a Manifestation of the Structure of the Neutron-Rich Nuclei

Dipole excitations in neutron-rich nuclei below the neutron threshold are investigated. The method is based on Hartree-Fock-Bogoliubov (HFB) and Quasiparticle-Phonon Model (QPM) theory. Of our special interest are the properties of the low-lying 1- Pygmy Resonance and the two-phonon quadrupole-octupole 1- states in Sn-isotopes including exploratory investigations for the experimentally unknown mass regions. In particular we investigate the evolution of the dipole strength function with the neutron excess. The use of HFB mean-field potentials and s.p. energies is found to provide a reliable extrapolation into the region off stability.Comment: 8 pages, 3 figures, Proceedings of the International Conference on Collective Motion in Nuclei Under Extreme Conditions (COMEX1), Paris, France, 10-13 June 200

Goishi tea consumption inhibits airway hyperresponsiveness in BALB/c mice

<p>Abstract</p> <p>Background</p> <p>Airway hyperresponsiveness (AHR) is one of the important traits that characterize bronchial asthma. Goishi tea is a post-heating fermented tea that has been reported to have higher free radical scavenging activity. In this study, we evaluated the prophylactic effects of Goishi tea on AHR in BALB/c mice.</p> <p>Results</p> <p>The number of inflammatory cells in BAL fluid was considerably reduced in Goishi tea/<it>Der f </it>and Gallic acid/<it>Der f </it>groups as compared with Tap water/<it>Der f </it>group. Regarding inflammatory cells in BAL, a significant reduction of eosinophils and neutrophils was observed in Goishi tea-treated mice (p < 0.01), as well as in the Gallic acid/<it>Der f </it>group (p < 0.05), as compared with Tap water/<it>Der f </it>group. In asthmatic mice (Tap water/<it>Der f </it>group), the intensity of airway resistance increased simultaneously with the increase in acetylcholine concentration in a dose-dependant way. AHR was significantly inhibited in Goishi tea/<it>Der f </it>and Gallic acid/<it>Der f </it>(p < 0.01) groups as compared with the Tap water/<it>Der f </it>group. Regarding serum specific-IgG₁, significantly lower levels of this antibody were observed in Goishi tea/<it>Der f </it>and Gallic acid/<it>Der f </it>groups as compared with the Tap water/<it>Der f </it>group (p < 0.05). In addition, adiponectin level was significantly higher in the Goishi tea group as compared with the Tap water treated mice (p < 0.01).</p> <p>Conclusions</p> <p>The results suggest that Goishi tea consumption exerted an inhibitory effect on eosinophilic and neutrophilic infiltration in the lung, attenuated the increase in airway resistance and increased the production of adiponectin; thus reducing Der f induced allergic inflammatory process in mice.</p

Roles of Heterochromatin and Telomere Proteins in Regulation of Fission Yeast Telomere Recombination and Telomerase Recruitment*

When the telomerase catalytic subunit (Trt1/TERT) is deleted, a majority of fission yeast cells survives by circularizing chromosomes. Alternatively, a small minority survives by maintaining telomeric repeats through recombination among telomeres. The recombination-based telomere maintenance in trt1Δ cells is inhibited by the telomere protein Taz1. In addition, catalytically inactive full-length Trt1 (Trt1-CI) and truncated Trt1 lacking the T-motif and reverse transcriptase (RT) domain (Trt1-ΔT/RT) can strongly inhibit recombination-based survival. Here, we investigated the effects of deleting the heterochromatin proteins Swi6 (HP1 ortholog) and Clr4 (Suv39 family of histone methyltransferases) and the telomere capping complex subunits Poz1 and Ccq1 on Taz1- and Trt1-dependent telomere recombination inhibition. The ability of Taz1 to inhibit telomere recombination did not require Swi6, Clr4, Poz1, or Ccq1. Although Swi6, Clr4, and Poz1 were dispensable for the inhibition of telomere recombination by Trt1-CI, Ccq1 was required for efficient telomere recruitment of Trt1 and Trt1-CI-dependent inhibition of telomere recombination. We also found that Swi6, Clr4, Ccq1, the checkpoint kinase Rad3 (ATR ortholog), and the telomerase regulatory subunit Est1 are all required for Trt1-ΔT/RT to inhibit telomere recombination. However, because loss of Swi6, Clr4, Rad3, Ccq1, or Est1 did not significantly alter the recruitment efficiency of Trt1-ΔT/RT to telomeres, these factors are likely to enhance the ability of Trt1-ΔT/RT to inhibit recombination-based survival by contributing to the negative regulation of telomere recombination