Prospects for Very High Energy Blazar Survey by the Next Generation Cherenkov Telescopes

The prospects for future blazar surveys by next-generation very high energy (VHE) gamma-ray telescopes, such as Advanced Gamma-ray Imaging System (AGIS) and Cherenkov Telescope Array (CTA), are investigated using the latest model of blazar luminosity function and its evolution which is in good agreement with the flux and redshift distribution of observed blazars as well as the extragalactic gamma-ray background. We extend and improve the template of spectral energy distributions (SEDs) based on the blazar SED sequence paradigm, to make it reliable also in the VHE bands (above 100 GeV) by comparing with the existing VHE blazar data. Assuming the planned CTA sensitivities, a blind survey using a total survey time of ~100 hrs could detect ~3 VHE blazars, with larger expected numbers for wider/shallower surveys. We also discuss following-up of Fermi blazars. Detectability of VHE blazars in the plane of Fermi flux and redshift is presented, which would be useful for future survey planning. Prospects and strategies are discussed to constrain the extragalactic background light (EBL) by using the absorption feature of brightest blazar spectra, as well as cut-offs in the redshift distribution. We will be able to get useful constraints on EBL by VHE blazars at different redshifts ranging 0.3-1 TeV corresponding to z=0.10-0.36.Comment: 11 pages, 11 figures, accepted for publication in PAS

Atiyah-Patodi-Singer index on a lattice

We propose a non-perturbative formulation of the Atiyah-Patodi-Singer(APS) index in lattice gauge theory, in which the index is given by the $\eta$ invariant of the domain-wall Dirac operator. Our definition of the index is always an integer with a finite lattice spacing. To verify this proposal, using the eigenmode set of the free domain-wall fermion, we perturbatively show in the continuum limit that the curvature term in the APS theorem appears as the contribution from the massive bulk extended modes, while the boundary $\eta$ invariant comes entirely from the massless edge-localized modes.Comment: 14 pages, appendices added, details of key equations added, typos corrected, to appear in PTE

Effect of 1,2-Dimethylhydrazine and Hydrogen Peroxide for the Duodenal Tumorigenesis in Relation to Blood Catalase Activity in Mice

Three different mouse strains, C3H/C^b_s C3H/HeN and B6C3 (C57BL x C3H) F1, having low, high and moderate catalase activities, were studied for duodenal tumorigenesis by the combined treatment with 1,2-dimethylhydrazine (DMH)* and hydrogen peroxide (HPO). DMH alone rarely induced duodenal tumors. Administration of HPO into 3 different mouse strains induced different frequencies of duodenal tumors ; 91.7% in C3H/C^b_s 9.5% in C3H/HeN and 31.8% in B6C3F1 mice. The incidence of duodenal tumors was significantly increased to 52.6% and 93.8% both in C3H/HeN and B6C3F1 mice by the combined administration of DMH and HPO. These increases in duodenal tumor were inversely correlated with the finding that administration of DMH or HPO alone or combined treatment of DMH and HPO significantly decreased mean blood catalase activities both in C3H and B6C3F1 mice

Gain-of-function oncogenic mutations in TP53 enhance defined factor-mediated cellular reprogramming

Cancer is a disorder with various genetic and epigenetic alterations. Genetic alterations such as mutations, i.e., substitutions, amplifications, and deletions of nucleotide sequences, are largely irreversible, whereas epigenetic alterations can be modified by pharmacological agents that target components of the epigenetic machinery. Recent studies have showed that introduction of defined factors such as those encoded by c-MYC, SOX2, OCT3/4, and KLF4 in normal somatic cells results in their dedifferentiation into induced pluripotent stem (iPS) cells. In addition, we have reported that these iPS factors induce the development of induced multipotent cancer (iPC) cells from gastrointestinal cancer cells by reducing tumor aggressiveness. The efficiency of iPS reprogramming increased when p53 was inhibited. The study of cancer cells suggests that the p53 pathways might be involved in the aggressive phenotypes of iPC cells in a long-term culture. However, the roles of gain-of-function oncogenic mutations in TP53, which is a key tumor suppressor gene, remain to be elucidated. We investigated reprogramming efficiency of iPS generation in human diploid fibroblasts that were co-transfected with TP53 mutants and defined factors. The results suggest that mutations in those TP53 regions that are involved in DNA contact might play a critical role in the efficiency of iPS generation. Taken together, our studies suggest 2 roles of TP53 mutations in reprogramming: (1) the structural mutations might contribute to, or collaborate with, other mutations to regulate the maintenance of genomic stability; (2) the DNA-contact mutations could affect the downstream target genes, which may be distinct from those involved in wild-type p53 function. These molecular manipulations of tumorigenicity and enhancement of cellular reprogramming efficiency by the p53 pathway will open an attractive and useful avenue for future medicine

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