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Comprehensive crash analysis includes calculating impact speed, which requires the determination of kinetic energy expended on the deformation of the vehicle's structural elements at the point of contact during a collision. The accuracy of the input data affects the resulting analysis of the crash. Therefore, this article aims to analyse selected factors influencing the determination of Energy Equivalent Speed (EES) determination using the CRASH3 algorithm: the extent of damage using defined measurement points, deformation width, and also limit speed b0. The variables were varied depending on selected factors such as the extent of damage, the type of collision (overlap), and also vehicle type (vehicle category classification). The presented study concluded that using 2 equally spaced measurement points to define the deformation profile should not be recommended in forensic practice when using CRASH3 algorithm. Using 7 measurement points seems more appropriate in case of equal spacing, even though the differences in calculated EES are not high when using 5 or 6 measurement points, especially with respect to the inaccuracy/technically acceptable tolerance of the EES value determination. The resulting EES is significantly influenced by variation of the deformation width. The used b0 range had a significant effect on the resulting EES value only in the case of SUVs. These vehicles show higher stiffness, which supposes the use of lower b0 values should not be recommended.

The Musashi family of RNA-binding proteins controls several biological processes including stem cell maintenance, cell division and neural function. Previously, we demonstrated that the C. elegans Musashi ortholog, msi-1, regulates forgetting via translational repression of the Arp2/3 actin-branching complex. However, the mechanisms controlling MSI-1 activity during the regulation of forgetting are currently unknown. Here we investigated the effects of protein phosphorylation on MSI-1 activity. We showed that MSI-1 function is likely controlled by alterations of its activity rather than its expression levels. Furthermore, we found that MSI-1 is phosphorylated and using mass spectrometry we identified MSI-1 phosphorylation at three residues (T18, S19 and S34). CRISPR-based manipulations of MSI-1 phosphorylation sites revealed that phosphorylation is necessary for MSI-1 function in both short- and long-term aversive olfactory associative memory. Thus, our study provides insight into the mechanisms regulating memory-related MSI-1 activity and may facilitate the development of novel therapeutic approaches. Author summary Understanding neural circuits and molecular mechanisms underlying learning and memory are the major challenges of neuroscience. It is a generally accepted model that a learning event causes modification of synapses; strengthening some within a circuit and weakening others (termed “synaptic plasticity”). A plastic nervous system requires not only the ability to acquire and store but also to forget new inputs. While learning and memory is widely investigated, clear-cut evidence for mechanisms involved in forgetting is still sparse. Previously, we demonstrated the role of the protein Musashi (MSI-1) in the active regulation of forgetting in the nematode C. elegans. Here we investigated the role of protein modification (phosphorylation) as a possible regulatory mechanism of the MSI-1 protein activity. We found that MSI-1 protein is modified at different positions and all of these modifications at the protein level contribute to the correct activity of the protein leading to active forgetting of short and long-term memories.

The Musashi family of RNA-binding proteins controls several biological processes including stem cell maintenance, cell division and neural function. Previously, we demonstrated that the C. elegans Musashi ortholog, msi-1, regulates forgetting via translational repression of the Arp2/3 actin-branching complex. However, the mechanisms controlling MSI-1 activity during the regulation of forgetting are currently unknown. Here we investigated the effects of protein phosphorylation on MSI-1 activity. We showed that MSI-1 function is likely controlled by alterations of its activity rather than its expression levels. Furthermore, we found that MSI-1 is phosphorylated and using mass spectrometry we identified MSI-1 phosphorylation at three residues (T18, S19 and S34). CRISPR-based manipulations of MSI-1 phosphorylation sites revealed that phosphorylation is necessary for MSI-1 function in both short- and long-term aversive olfactory associative memory. Thus, our study provides insight into the mechanisms regulating memory-related MSI-1 activity and may facilitate the development of novel therapeutic approaches.

Meiosis in angiosperm plants is followed by mitotic divisions to form multicellular haploid gametophytes. Termination of meiosis and transition to gametophytic development is, in Arabidopsis, governed by a dedicated mechanism that involves SMG7 and TDM1 proteins. Mutants carrying the smg7-6 allele are semi-fertile due to reduced pollen production. We found that instead of forming tetrads, smg7-6 pollen mother cells undergo multiple rounds of chromosome condensation and spindle assembly at the end of meiosis, resembling aberrant attempts to undergo additional meiotic divisions. A suppressor screen uncovered a mutation in centromeric histone H3 (CENH3) that increased fertility and promoted meiotic exit in smg7-6 plants. The mutation led to inefficient splicing of the CENH3 mRNA and a substantial decrease of CENH3, resulting in smaller centromeres. The reduced level of CENH3 delayed formation of the mitotic spindle but did not have an apparent effect on plant growth and development. We suggest that impaired spindle re-assembly at the end of meiosis limits aberrant divisions in smg7-6 plants and promotes formation of tetrads and viable pollen. Furthermore, the mutant with reduced level of CENH3 was very inefficient haploid inducer indicating that differences in centromere size is not the key determinant of centromere-mediated genome elimination.