In this project, different fission models in the nuclear reaction code TALYS have been compared to GEF version 2020/1.2. The data included in the comparison are mass yield distributions, average prompt neutron energies per fragment mass, and average multiplicities of both neutrons and γ-rays per fragment mass. The reaction studied in the first part of the project is 1 keV neutron-induced fission of 235U. In the second part of the study, a variety of different nuclei and different incident energies were included in comparisons, but a limitation was set to only include neutron-induced fission. The results from the comparison suggested that TALYS fymodel 2 and 3 were less consistent with GEF than fymodel 4. For the comparisons with experimental data, fymodel 4 also performed better overall. TALYS fymodel 2 and 3 make use of implemented partial versions of GEF to produce fission fragment distributions, while fymodel 4 takes fission fragment distribution data from separate yieldfiles. A database of these yieldfiles with 737 different nuclei and 10 energy levels was produced, to be implemented in future versions of TALYS. The energy levels were chosen to get a range of energies that can be accurately interpolated between. This method of using TALYS fymodel 4 with a yieldfile from GEF consistently showed a strong agreement with GEF version 2020/1.2 for the mass yield distributions and the neutron multiplicities. The γ-ray multiplicities and the neutron energies show a slightly weaker agreement, and TALYS gives consistently smaller values than GEF for these quantities.

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Independent yield distributions of high-energy neutron-induced fission are of importance to achieve a good understanding of fission. Even though the mass and charge yield distributions of thermal neutron-induced fission are well known, there are few experimental data for high-energy neutron-induced fission. In addition to basic research on the fission process, independent yield distributions of high-energy neutron-induced fission play a key role in the development of Generation IV fast nuclear reactors. To facilitate measurements of independent fission yields of high-energy neutron-induced fission, a dedicated ion guide and a proton-neutron converter were developed and put to use in experiments at the isotope separator facility IGISOL in Jyväskylä. In parallel, a simulation model of the system was developed in order to optimize the collecting efficiency of fission products in the ion guide. The model uses the Monte Carlo code MCNPX to simulate the neutron production, the fission model code GEF to simulate the fission process, and GEANT4 for ion transportation. In order to benchmark the simulation model, metal foils were inserted in the ion guide with the purpose of collecting fission products. At the same time, nickel, cobalt and indium foils were located between the pn-converter and the ion guide to record the neutron flux from the pn-converter. After the beam was turned off, and after several days of cooling, g-ray spectroscopy measurements of the foils were conducted using a well shielded HPGe detector. Based on the identified g-ray transitions in the spectroscopy data, the productions of corresponding fission products and neutron activation products were calculated, and then used to benchmark the transportation and collection of fission products, as well as neutron production, in the simulations. The conclusion from the benchmark is that the transportation of fission products in the helium gas, as simulated by GEANT4, agrees very well with the measurement, while the transportation of fission products in the uranium targets agrees with the measurement within 10%. The neutron flux at the high-energy part of the neutron spectrum is overestimated by about 40%.Thanks to the benchmark it has been shown that the predictive power of the model is satisfactory and sufficient for the purpose of modeling the ion guide. Furthermore, the parameters involved in the simulations, such as neutron production, distance between the neutron source and the ion guide, volume of the ion guide and so on, play an important role in the optimization of the setup. However, the lower than expected fission rate suggests that the optimization on these parameters may not be enough to achieve a sufficiently high intensity of fission products, especially for nuclei far from the stability line. To achieve a sufficiently high intensity, an electric field guidance, similar to the RF structure of the CARIBU gas catcher presented in G.Savard et al. Nucl. Inst. Meth. B, 376: 246, 2016, to collect fission products is considered.

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The Rho family small GTPases are key regulators of the cytoskeleton, through which they impact and control many vital cellular functions, including growth, vesicle trafficking, intercellular junctions, transepithelial transport, migration, and gene transcription. Activation of Rho GTPases is induced by Guanine Nucleotide Exchange Factors (GEFs). We have previously shown that Tumour Necrosis Factor-α (TNF), plasma membrane depolarization, and immunosuppressive drugs activate RhoA through a specific exchange factor, GEF-H1. However, the question of whether other stimuli, such as hyperosmolarity, that activate RhoA, act through GEF-H1 and whether GEF-H1 activates other RhoGTPases was not known. The overall objective of this research project has been to gain insights into the complex mechanism through which the Rho GTPases, Rac and RhoA, are regulated in tubular cells. Specifically, we wished to explore the role and pathway-specific regulation of GEF-H1 in hyperosmotic stress- and TNF-induced signalling in tubular cells. In order to accomplish our goals, we optimized and used affinity precipitation assays to detect GEF-H1 activation (RhoA(G17A) and Rac(G15A)). We found that 1) GEF-H1 is activated by hyperosmotic stress and mediates the hyperosmolarity-induced RhoA activation, as well as nuclear translocation of the Myocardin-Related Transcription Factor (MRTF); 2) TNF induces activation of both Rac and RhoA through GEF-H1, but via different mechanisms. Epidermal Growth Factor Receptor (EGFR)- and Extracellular signal Regulated Kinase (ERK)-dependent phosphorylation at the Thr678 site of GEF-H1 is a prerequisite for RhoA activation only, while both Rac and RhoA activation require GEF-H1 phosphorylation on Ser885. Interestingly, Rac is required for TNF-induced RhoA activation. Together these findings highlight a role for GEF-H1 as an osmosensitive molecule that regulates cellular reprogramming through MRTF. Importantly, we have also uncovered a novel mechanism explaining hierarchical activation of Rac and RhoA by TNF. Such a mechanism could be key in coordinating GEF function and fine-tuning Rac and RhoA activation.

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