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- Allahverdi, Rouzbeh, et al.
(författare)
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Lepton flavor violation at the Large Hadron Collider
- 2012
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Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; 86:1, s. 015026-
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Tidskriftsartikel (refereegranskat)abstract
- We investigate a potential of discovering lepton flavor violation (LFV) at the Large Hadron Collider. A sizeable LFV in low energy supersymmetry can be induced by massive right-handed neutrinos, which can explain neutrino oscillations via the seesaw mechanism. We investigate a scenario where the distribution of an invariant mass of two hadronically decaying taus (tau(h)tau(h)) from (chi) over bar (0)(2) decays is the same in events with or without LFV. We first develop a transfer function using this ditau mass distribution to model the shape of the non-LFV tau(h)mu invariant mass. We then show the feasibility of extracting the LFV tau(h)mu signal. The proposed technique can also be applied for a LFV tau(h)e search.
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2. |
- Dutta, Bhaskar, et al.
(författare)
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Diagnosis of supersymmetry breaking mediation schemes by mass reconstruction at the LHC
- 2012
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Ingår i: Physical Review D. - 1550-7998 .- 1550-2368. ; 85:11, s. 115007-
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Tidskriftsartikel (refereegranskat)abstract
- If supersymmetry is discovered at the LHC, the next question will be the determination of the underlying model. While this may be challenging or even intractable, a more optimistic question is whether we can understand the main contours of any particular paradigm of the mediation of supersymmetry breaking. The determination of superpartner masses through endpoint measurements of kinematic observables arising from cascade decays is a powerful diagnostic tool. In particular, the determination of the gaugino sector has the potential to discriminate between certain mediation schemes (not all schemes, and not between different UV realizations of a given scheme). We reconstruct gaugino masses, choosing a model where anomaly contributions to supersymmetry breaking are important (KKLT compactification), and find the gaugino unification scale. Moreover, reconstruction of other superpartner masses allows us to solve for the parameters defining the UV model. The analysis is performed in the stop and stau coannihilation regions where the lightest neutralinos are mainly gauginos, to additionally satisfy dark matter constraints. We thus develop observables to determine stau and stop masses to verify that the coannihilation mechanism is indeed operational, and solve for the relic density.
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3. |
- Maurer, Matthew, et al.
(författare)
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3-Phosphoinositide-dependent kinase 1 potentiates upstream lesions on the phosphatidylinositol 3-kinase pathway in breast carcinoma
- 2009
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Ingår i: Cancer Research. - 1538-7445. ; 69:15, s. 306-6299
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Tidskriftsartikel (refereegranskat)abstract
- Lesions of ERBB2, PTEN, and PIK3CA activate the phosphatidylinositol 3-kinase (PI3K) pathway during cancer development by increasing levels of phosphatidylinositol-3,4,5-triphosphate (PIP(3)). 3-Phosphoinositide-dependent kinase 1 (PDK1) is the first node of the PI3K signal output and is required for activation of AKT. PIP(3) recruits PDK1 and AKT to the cell membrane through interactions with their pleckstrin homology domains, allowing PDK1 to activate AKT by phosphorylating it at residue threonine-308. We show that total PDK1 protein and mRNA were overexpressed in a majority of human breast cancers and that 21% of tumors had five or more copies of the gene encoding PDK1, PDPK1. We found that increased PDPK1 copy number was associated with upstream pathway lesions (ERBB2 amplification, PTEN loss, or PIK3CA mutation), as well as patient survival. Examination of an independent set of breast cancers and tumor cell lines derived from multiple forms of human cancers also found increased PDK1 protein levels associated with such upstream pathway lesions. In human mammary cells, PDK1 enhanced the ability of upstream lesions to signal to AKT, stimulate cell growth and migration, and rendered cells more resistant to PDK1 and PI3K inhibition. After orthotopic transplantation, PDK1 overexpression was not oncogenic but dramatically enhanced the ability of ERBB2 to form tumors. Our studies argue that PDK1 overexpression and increased PDPK1 copy number are common occurrences in cancer that potentiate the oncogenic effect of upstream lesions on the PI3K pathway. Therefore, we conclude that alteration of PDK1 is a critical component of oncogenic PI3K signaling in breast cancer.
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