Search for the Higgs boson produced in association with Z-->l+l in pp collisions at sqrt[s]=1.96 TeV.

Division of High Energy Physics, Department of Physics, University of Helsinki and Helsinki Institute of Physics, FIN-00014, Helsinki, Finland.
Physical Review Letters (Impact Factor: 7.51). 12/2008; 101(25):251803.
Source: PubMed


We present a search for the Higgs boson in the process qq-->ZH-->l;{+}l;{-}bb[over ]. The analysis uses an integrated luminosity of 1 fb;{-1} of pp[over ] collisions produced at sqrt[s]=1.96 TeV and accumulated by the upgraded Collider Detector at Fermilab (CDF II). We employ artificial neural networks both to correct jets mismeasured in the calorimeter and to distinguish the signal kinematic distributions from those of the background. We see no evidence for Higgs boson production, and set 95% C.L. upper limits on sigma{ZH}B(H-->bb[over ]), ranging from 1.5 to 1.2 pb for a Higgs boson mass (m{H}) of 110 to 150 GeV/c(2).

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    ABSTRACT: Human papilloma virus type 16 (HPV16) E7 is a viral oncoprotein that is believed to play a major role in cervical neoplasia. A novel antagonist peptide against HPV16 E7 was previously selected by phage display screening and the selected peptide was found to have anti-tumor efficacy against HPV16-positive cervical carcinoma through induction of cell cycle arrest. In the current study, to further elucidate the mechanisms of the antagonist peptide, the effects of the peptide on apoptosis are investigated by RT-PCR, Western blotting, MTT assay, TUNEL staining, Annexin V apoptosis assay, flow cytometry, and animal experiments. The antagonist peptide showed obvious anti-tumor efficacy through apoptosis induction, both in HPV16-positive cervical cancer cell lines and tumor xenografts. Our results also revealed that the peptide induced accumulation of cellular p53 and p21, and led to HPV16 E7 protein degradation. In the case of mRNA levels, it resulted in unaltered p53 and HPV16 E7 expression, but increased expression of p21. In contrast, the induction of apoptosis and p53 reactivation effects by the selected peptide were abolished after E7 knocked down with siRNA. These results demonstrate that the selected peptide can induce E7 degradation and lead to marked apoptosis in HPV16-related cancer cells by activating cellular p53 and its target genes, such as p21. Furthermore, the evident therapeutic efficacy obtained from the subcutaneous tumor model experiments in nude mice suggests a therapeutic potential for HPV16-related cancers of the selected peptide. Therefore, this specific peptide may be used to create specific biotherapies for the treatment of HPV 16-positive cervical cancers.
    No preview · Article · Jun 2011 · Apoptosis