Heavy Vector-like Top Partners at the LHC and flavour constraints

We consider the phenomenology at the Large Hadron Collider of new heavy vector-like quarks which couple mainly to the third generation quarks via Yukawa interactions, with special emphasis on non-standard doublet representations which are less constrained from present data. We also discuss in detail the flavour limits at tree level and loop level and implications of a generalised CKM mixing matrix to these cases.Comment: 45 pages, 20 figures, 8 tables. Updated limits in the B-physics part, typos corrected, minor modifications in the LHC par

変異FGFR３の恒常的リン酸化は先天性小人症の重要な因子でPLCγによるSTAT1の活性化を介して軟骨前駆細胞ATDC5のアポトーシスを誘導する

The most frequent type of rhizomelic dwarfism, achondroplasia (ACH), is caused by mutations in the fibroblast growth factor receptor 3 (FGFR3) gene. Mutations in FGFR3 result in skeletal dysplasias of variable severity, including mild phenotypic effects in hypochondroplasia (HCH), severe phenotypic effects in thanatophoric dysplasia types I (TDI) and II (TDII), and severe but survivable phenotypic effects in severe achondroplasia with developmental delay and acanthosis nigricans (SADDAN). To explore the molecular mechanisms that result in the different phenotypes, we investigated the kinetics of mutated versions of FGFR3. First, we assayed the phosphorylation states of the mutated FGFR3s and found that the level of phosphorylation in TDI-FGFR3 was lower than in ACH-FGFR3, although the other mutants were phosphorylated according to phenotypic severity. Second, we analyzed the duration of the phosphorylation. TDI-FGFR3 was not highly phosphorylated under ligand-free conditions, but the peak phosphorylation levels of TDI-FGFR3 and ACH-FGFR3 were maintained for 30 min after stimulation with FGF-1. Moreover, ligand-dependent phosphorylation of TDI-FGFR3, but not ACH-FGFR3, lasted for more than 8 h after FGF-1 administration. The other mutant proteins showed sustained phosphorylation independent of ligand presence. Third, we investigated the intracellular localization of the mutant proteins. Immunofluorescence analysis showed accumulations of TDII-FGFR3, SADDAN-FGFR3, and a portion of TDI-FGFR3 in the endoplasmic reticulum (ER). Based on these data, we concluded that sustained phosphorylation of FGFR3 causes chondrodysplasia, and the phenotypic severity depends on the proportion of ER-localized mutant FGFR3. In FGFR3 signaling, the transcription factor, signal transducer and activator of transcription 1 (STAT1) inhibit proliferation and induce apoptosis of chondrocytes. Here we reveal that phospholipase C gamma (PLCgamma) mediates FGFR3-induced STAT1 activation. Both PLCgamma and STAT1 were activated by FGFR3 signaling, but a dominant-negative form of PLCgamma (DN-PLCgamma) remarkably reduced STAT1 phosphorylation. Apoptosis assays revealed that the constitutively active forms of FGFR3 (TDII-FGFR3) and STAT1 (STAT1-C) induce apoptosis of chondrogenic ATDC5 cells via caspase activity. DN-PLCgamma reduced the apoptosis of ATDC5 cells expressing TDII-FGFR3, but over-expression of both DN-PLCgamma and STAT1-C induced apoptosis. Therefore, we conclude that a PLCgamma-STAT1 pathway mediates apoptotic signaling by FGFR3

A feasibility study of the measurement of Higgs pair creation at a Photon Linear Collider

We studied the feasibility of the measurement of Higgs pair creation at a Photon Linear Collider (PLC). From the sensitivity to the anomalous self-coupling of the Higgs boson, the optimum $\gamma \gamma$ collision energy was found to be around 270 GeV for a Higgs mass of 120 GeV/$c^2$. We found that large backgrounds such as $\gamma \gamma \rightarrow W^+W^-, ZZ,$ and $b\bar{b}b\bar{b}$, can be suppressed if correct assignment of tracks to parent partons is achieved and Higgs pair events can be observed with a statistical significance of $\sim 5 \sigma$ by operating the PLC for 5 years.Comment: 7 pages, 8 figures, 5 table