Towards a predictive multi-phase model for alpine mass movements and process cascades

Alpine mass movements can generate process cascades involving different materials including rock, ice, snow, and water. Numerical modelling is an essential tool for the quantification of natural hazards. Yet, state-of-the-art operational models are based on parameter back-calculation and thus reach their limits when facing unprecedented or complex events. Here, we advance our predictive capabilities for mass movements and process cascades on the basis of a three-dimensional numerical model, coupling fundamental conservation laws to finite strain elastoplasticity. In this framework, model parameters have a true physical meaning and can be evaluated from material testing, thus conferring to the model a strong predictive nature. Through its hybrid Eulerian–Lagrangian character, our approach naturally reproduces fractures and collisions, erosion/deposition phenomena, and multi-phase interactions, which finally grant accurate simulations of complex dynamics. Four benchmark simulations demonstrate the physical detail of the model and its applicability to real-world full-scale events, including various materials and ranging through five orders of magnitude in volume. In the future, our model can support risk-management strategies through predictions of the impact of potentially catastrophic cascading mass movements at vulnerable sites

The phenotypes of temperature-sensitive mini-RK2 replicons carrying mutations in the replication control gene trfA are suppressed nonspecifically by intragenic cop mutations.

The minimal replicon of the broad-host-range plasmid RK2 consists of the origin of vegetative replication (oriV) and a gene (trfA) encoding an essential replication protein that binds to short repeats in oriV. We report here the results of a DNA sequence analysis of seven unique mutants that are temperature sensitive for replication in Escherichia coli. The mutations (designated rts) were distributed throughout 40% of the downstream part of the trfA gene. Spontaneous revertants of the rts mutants were isolated, and further analysis of four such revertants demonstrated that the new phenotypes resulted from intragenic second-site copy up (cop) mutations. Subcloning experiments showed that all tested intragenic combinations of rts and cop mutations resulted in elimination or strong reduction of the temperature sensitivity of replication. This suppression was also observed under conditions where the mutant TrfA protein was provided in trans with respect to oriV, indicating that the reduction in temperature sensitivity could not be a TrfA protein dosage effect. The phenotypes of two of the cop mutants in Pseudomonas aeruginosa were analyzed; the results demonstrated that the mutants were either not functional or poorly functional in this host. The rts mutant plasmids were also reduced in their ability to replicate in P. aeruginosa, and the intragenic cop mutations did not improve the functionality of these mutants. The significance of the results is discussed in relation to current models of the mechanism of action of the TrfA protein