| 1. |
- Barausse, Enrico, et al.
(author)
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Prospects for fundamental physics with LISA
- 2020
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In: General Relativity and Gravitation. - : SPRINGER/PLENUM PUBLISHERS. - 0001-7701 .- 1572-9532. ; 52:8
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Journal article (other academic/artistic)abstract
- In this paper, which is of programmatic rather than quantitative nature, we aim to further delineate and sharpen the future potential of the LISA mission in the area of fundamental physics. Given the very broad range of topics that might be relevant to LISA,we present here a sample of what we view as particularly promising fundamental physics directions. We organize these directions through a "science-first" approach that allows us to classify how LISA data can inform theoretical physics in a variety of areas. For each of these theoretical physics classes, we identify the sources that are currently expected to provide the principal contribution to our knowledge, and the areas that need further development. The classification presented here should not be thought of as cast in stone, but rather as a fluid framework that is amenable to change with the flow of new insights in theoretical physics.
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| 2. |
- Agredo Chavez, Angelica Maria, et al.
(author)
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Structural model updating of an existing concrete bridge based on load testing and monitoring data
- 2023
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In: Life-Cycle of Structures and Infrastructure Systems. - : Taylor & Francis Group. - 9781003323020 ; , s. 3999-4006
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Conference paper (other academic/artistic)abstract
- The backbone of European infrastructure was built after the end of the second World War and has reached, or is near to, the end of its nominal design life. This issue urges the development of structural assessment procedures that can provide infrastructure managers the information to make decisions for repairing, upgrading, or replacement. In this paper, a methodology based on load testing and Structural Health Monitoring (SHM) for the assessment of a 65- year-old prestressed concrete bridge located in Northern Sweden is presented. The retrieved data is used to develop and calibrate structural models with different levels of data completeness. The SHM procedure includes the evaluation of material properties by diagnostics, definition of the layout and installation of the instrumentation, test execution, and data analysis. A preliminary structural model is developed based only on the original design parameters, and it is sequentially updated with monitoring data retrieved during a performed proof loading test of the bridge.
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| 3. |
- Iadevaia, V., et al.
(author)
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PIM1 kinase is destabilized by ribosomal stress causing inhibition of cell cycle progression
- 2010
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In: Oncogene. - : Springer Science and Business Media LLC. - 1476-5594 .- 0950-9232. ; 29:40, s. 5490-5499
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Journal article (peer-reviewed)abstract
- PIM1 is a constitutively active serine/threonine kinase regulated by cytokines, growth factors and hormones. It has been implicated in the control of cell cycle progression and apoptosis and its overexpression has been associated with various kinds of lymphoid and hematopoietic malignancies. The activity of PIM1 is dependent on the phosphorylation of several targets involved in transcription, cell cycle and apoptosis. We have recently observed that PIM1 interacts with ribosomal protein (RP) S19 and cosediments with ribosomes. Defects in ribosome synthesis (ribosomal stress) have been shown to activate a p53-dependent growth arrest response. To investigate if PIM1 could have a role in the response to ribosomal stress, we induced ribosome synthesis alterations in TF-1 and K562 erythroid cell lines. We found that RP deficiency, induced by RNA interference or treatment with inhibitor of nucleolar functions, causes a drastic destabilization of PIM1. The lower level of PIM1 induces an increase in the cell cycle inhibitor p27(Kip1) and blocks cell proliferation even in the absence of p53. Notably, restoring PIM1 level by transfection causes a recovery of cell growth. Our data indicate that PIM1 may act as a sensor for ribosomal stress independently of or in concert with the known p53-dependent mechanisms. Oncogene (2010) 29, 5490-5499; doi:10.1038/onc.2010.279; published online 19 July 2010
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