Effects of CP-violating phases in supersymmetry

Recent studies about the impact of the CP-violating complex parameters in supersymmetry on the decays of third generation squarks and about T-odd asymmetries in neutralino and chargino production and decay are reviewed. The CP-even branching ratios of the third generation squarks show a pronounced dependence on the phases of A_t, A_b, mu and M_1 in a large region of the supersymmetric parameter space. This could have important implications for stop and sbottom searches and the MSSM parameter determination in future collider experiments. We have estimated the expected accuracy in the determination of the parameters by global fits of measured masses, decay branching ratios and production cross sections. We have found that the parameter A_t can be determined with an error of 2 - 3%, whereas the error on A_b is likely to be of the order of 50 - 100%. In addition we have studied CP-odd observables, like asymmetries based on triple product correlations, which are necessary to unambiguously establish CP violation. We have analysed these asymmetries in neutralino and chargino production with subsequent three-body decays at the International Linear Collider with longitudinally polarised beams in the MSSM with complex parameters M_1 and mu. The asymmetries, which appear already at tree-level because of spin correlation between production and decay, can be as large as 20% and will therefore be an important tool for the search for CP-violating effects in supersymmetry.Comment: 13 pages, LaTeX, 7 eps figures, uses appolb.cls, presented at the final meeting of the European Network ``Physics at Colliders'', Montpellier, September 26 - 27, 200

A scheme with two large extra dimensions confronted with neutrino physics

We investigate a particle physics model in a six-dimensional spacetime, where two extra dimensions form a torus. Particles with Standard Model charges are confined by interactions with a scalar field to four four-dimensional branes, two vortices accommodating ordinary type fermions and two antivortices accommodating mirror fermions. We investigate the phenomenological implications of this multibrane structure by confronting the model with neutrino physics data.Comment: LATEX, 24 pages, 9 figures, minor changes in the tex

Resistance of Gram-positive bacteria to nisin is not determined by Lipid II levels

Lipid II is essential for nisin-mediated pore formation at nano-molar concentrations. We tested whether nisin resistance could result from different Lipid II levels, by comparing the maximal Lipid II pool in Micrococcus flavus (sensitive) and Listeria monocytogenes (relatively insensitive) and their nisin-resistant variants, with a newly developed method. No correlation was observed between the maximal Lipid II pool and nisin sensitivity, as was further corroborated by using spheroplasts of nisin-resistant and wild-type strains of M. flavus, which were equally sensitive to nisin. (C) 2004 Federation of European Microbiological Societies. Published by Elsevier B.V. All rights reserved

The hypoxic cancer secretome induces pre-metastatic bone lesions through lysyl oxidase

Tumour metastasis is a complex process involving reciprocal interplay between cancer cells and host stroma at both primary and secondary sites, and is strongly influenced by microenvironmental factors such as hypoxia. Tumour-secreted proteins play a crucial role in these interactions and present strategic therapeutic potential. Metastasis of breast cancer to the bone affects approximately 85% of patients with advanced disease and renders them largely untreatable. Specifically, osteolytic bone lesions, where bone is destroyed, lead to debilitating skeletal complications and increased patient morbidity and mortality. The molecular interactions governing the early events of osteolytic lesion formation are currently unclear. Here we show hypoxia to be specifically associated with bone relapse in patients with oestrogen-receptor negative breast cancer. Global quantitative analysis of the hypoxic secretome identified lysyl oxidase (LOX) as significantly associated with bone-tropism and relapse. High expression of LOX in primary breast tumours or systemic delivery of LOX leads to osteolytic lesion formation whereas silencing or inhibition of LOX activity abrogates tumour-driven osteolytic lesion formation. We identify LOX as a novel regulator of NFATc1-driven osteoclastogenesis,independent of RANK ligand, which disrupts normal bone homeostasisleading to the formation of focal pre-metastatic lesions. We show that these lesions subsequently provide a platform for circulating tumour cells to colonize and form bone metastases. Our study identifies a novel mechanism of regulation of bone homeostasis and metastasis, opening up opportunities for novel therapeutic intervention with important clinical implications