User Experience Design for E-Voting: How mental models align with security mechanisms

This paper presents a mobile application for vote-casting and vote-verification based on the Selene e-voting protocol and explains how it was developed and implemented using the User Experience Design process. The resulting interface was tested with 38 participants, and user experience data was collected via questionnaires and semi-structured interviews on user experience and perceived security. Results concerning the impact of displaying security mechanisms on UX were presented in a complementary paper. Here we expand on this analysis by studying the mental models revealed during the interviews and compare them with theoretical security notions. Finally, we propose a list of improvements for designs of future voting protocols.Comment: E-Vote-ID 2019 TalTech Proceeding

Towards higher order lattice Boltzmann schemes

In this contribution we extend the Taylor expansion method proposed previously by one of us and establish equivalent partial differential equations of DDH lattice Boltzmann scheme at an arbitrary order of accuracy. We derive formally the associated dynamical equations for classical thermal and linear fluid models in one to three space dimensions. We use this approach to adjust relaxation parameters in order to enforce fourth order accuracy for thermal model and diffusive relaxation modes of the Stokes problem. We apply the resulting scheme for numerical computation of associated eigenmodes and compare our results with analytical references

Interest of colchicine for the treatment of cystic fibrosis patients. Preliminary report.

Cystic fibrosis (CF) lung disease is characterized by persistent inflammation. Antiinflammatory drugs, such as corticosteroids and ibuprofen, have proved to slow the decline of pulmonary function although their use is limited because of frequent adverse events. We hypothesized that colchicine could be an alternative treatment because of its antiinflammatory properties and upregulatory effect on cystic fibrosis transmembrane regulator (CFTR) closely related proteins. We herein present results obtained in an open study of eight CF children treated with colchicine for at least 6 months. Clinical status was better in all patients and respiratory function tests significantly improved in five. Median duration of antibiotherapy decreased significantly. These preliminary results support our hypothesis of a beneficial effect of colchicine in CF patients and stress the need for a controlled therapeutic trial

On the Three-dimensional Central Moment Lattice Boltzmann Method

A three-dimensional (3D) lattice Boltzmann method based on central moments is derived. Two main elements are the local attractors in the collision term and the source terms representing the effect of external and/or self-consistent internal forces. For suitable choices of the orthogonal moment basis for the three-dimensional, twenty seven velocity (D3Q27), and, its subset, fifteen velocity (D3Q15) lattice models, attractors are expressed in terms of factorization of lower order moments as suggested in an earlier work; the corresponding source terms are specified to correctly influence lower order hydrodynamic fields, while avoiding aliasing effects for higher order moments. These are achieved by successively matching the corresponding continuous and discrete central moments at various orders, with the final expressions written in terms of raw moments via a transformation based on the binomial theorem. Furthermore, to alleviate the discrete effects with the source terms, they are treated to be temporally semi-implicit and second-order, with the implicitness subsequently removed by means of a transformation. As a result, the approach is frame-invariant by construction and its emergent dynamics describing fully 3D fluid motion in the presence of force fields is Galilean invariant. Numerical experiments for a set of benchmark problems demonstrate its accuracy.Comment: 55 pages, 8 figure

SUMO chain formation is required for response to replication arrest in S. pombe

SUMO is a ubiquitin-like protein that is post-translationally attached to one or more lysine residues on target proteins. Despite having only 18% sequence identity with ubiquitin, SUMO contains the conserved betabetaalphabetabetaalphabeta fold present in ubiquitin. However, SUMO differs from ubiquitin in having an extended N-terminus. In S. pombe the N-terminus of SUMO/Pmt3 is significantly longer than those of SUMO in S. cerevisiae, human and Drosophila. Here we investigate the role of this N-terminal region. We have used two dimensional gel electrophoresis to demonstrate that S. pombe SUMO/Pmt3 is phosphorylated, and that this occurs on serine residues at the extreme N-terminus of the protein. Mutation of these residues (in pmt3-1) results in a dramatic reduction in both the levels of high Mr SUMO-containing species and of total SUMO/Pmt3, indicating that phosphorylation of SUMO/Pmt3 is required for its stability. Despite the significant reduction in high Mr SUMO-containing species, pmt3-1 cells do not display an aberrant cell morphology or sensitivity to genotoxins or stress. Additionally, we demonstrate that two lysine residues in the N-terminus of S. pombe SUMO/Pmt3 (K14 and K30) can act as acceptor sites for SUMO chain formation in vitro. Inability to form SUMO chains results in aberrant cell and nuclear morphologies, including stretched and fragmented chromatin. SUMO chain mutants are sensitive to the DNA synthesis inhibitor, hydroxyurea (HU), but not to other genotoxins, such as UV, MMS or CPT. This implies a role for SUMO chains in the response to replication arrest in S. pomb

Cytoplasmic PML promotes TGF-β-associated epithelial–mesenchymal transition and invasion in prostate cancer

Epithelial–mesenchymal transition (EMT) is a key event that is involved in the invasion and dissemination of cancer cells. Although typically considered as having tumour-suppressive properties, transforming growth factor (TGF)-β signalling is altered during cancer and has been associated with the invasion of cancer cells and metastasis. In this study, we report a previously unknown role for the cytoplasmic promyelocytic leukaemia (cPML) tumour suppressor in TGF-β signalling-induced regulation of prostate cancer-associated EMT and invasion. We demonstrate that cPML promotes a mesenchymal phenotype and increases the invasiveness of prostate cancer cells. This event is associated with activation of TGF-β canonical signalling pathway through the induction of Sma and Mad related family 2 and 3 (SMAD2 and SMAD3) phosphorylation. Furthermore, the cytoplasmic localization of promyelocytic leukaemia (PML) is mediated by its nuclear export in a chromosomal maintenance 1 (CRM1)-dependent manner. This was clinically tested in prostate cancer tissue and shown that cytoplasmic PML and CRM1 co-expression correlates with reduced disease-specific survival. In summary, we provide evidence of dysfunctional TGF-β signalling occurring at an early stage in prostate cancer. We show that this disease pathway is mediated by cPML and CRM1 and results in a more aggressive cancer cell phenotype. We propose that the targeting of this pathway could be therapeutically exploited for clinical benefit

Placental syncytiotrophoblast constitutes a major barrier to vertical transmission of Listeria monocytogenes.

Listeria monocytogenes is an important cause of maternal-fetal infections and serves as a model organism to study these important but poorly understood events. L. monocytogenes can infect non-phagocytic cells by two means: direct invasion and cell-to-cell spread. The relative contribution of each method to placental infection is controversial, as is the anatomical site of invasion. Here, we report for the first time the use of first trimester placental organ cultures to quantitatively analyze L. monocytogenes infection of the human placenta. Contrary to previous reports, we found that the syncytiotrophoblast, which constitutes most of the placental surface and is bathed in maternal blood, was highly resistant to L. monocytogenes infection by either internalin-mediated invasion or cell-to-cell spread. Instead, extravillous cytotrophoblasts-which anchor the placenta in the decidua (uterine lining) and abundantly express E-cadherin-served as the primary portal of entry for L. monocytogenes from both extracellular and intracellular compartments. Subsequent bacterial dissemination to the villous stroma, where fetal capillaries are found, was hampered by further cellular and histological barriers. Our study suggests the placenta has evolved multiple mechanisms to resist pathogen infection, especially from maternal blood. These findings provide a novel explanation why almost all placental pathogens have intracellular life cycles: they may need maternal cells to reach the decidua and infect the placenta

Dynamics of fluctuations in a fluid below the onset of Rayleigh-B\'enard convection

We present experimental data and their theoretical interpretation for the decay rates of temperature fluctuations in a thin layer of a fluid heated from below and confined between parallel horizontal plates. The measurements were made with the mean temperature of the layer corresponding to the critical isochore of sulfur hexafluoride above but near the critical point where fluctuations are exceptionally strong. They cover a wide range of temperature gradients below the onset of Rayleigh-B\'enard convection, and span wave numbers on both sides of the critical value for this onset. The decay rates were determined from experimental shadowgraph images of the fluctuations at several camera exposure times. We present a theoretical expression for an exposure-time-dependent structure factor which is needed for the data analysis. As the onset of convection is approached, the data reveal the critical slowing-down associated with the bifurcation. Theoretical predictions for the decay rates as a function of the wave number and temperature gradient are presented and compared with the experimental data. Quantitative agreement is obtained if allowance is made for some uncertainty in the small spacing between the plates, and when an empirical estimate is employed for the influence of symmetric deviations from the Oberbeck-Boussinesq approximation which are to be expected in a fluid with its density at the mean temperature located on the critical isochore.Comment: 13 pages, 10 figures, 52 reference

Role of mitochondrial raft-like microdomains in the regulation of cell apoptosis

Lipid rafts are envisaged as lateral assemblies of specific lipids and proteins that dissociate and associate rapidly and form functional clusters in cell membranes. These structural platforms are not confined to the plasma membrane; indeed lipid microdomains are similarly formed at subcellular organelles, which include endoplasmic reticulum, Golgi and mitochondria, named raft-like microdomains. In addition, some components of raft-like microdomains are present within ER-mitochondria associated membranes. This review is focused on the role of mitochondrial raft-like microdomains in the regulation of cell apoptosis, since these microdomains may represent preferential sites where key reactions take place, regulating mitochondria hyperpolarization, fission-associated changes, megapore formation and release of apoptogenic factors. These structural platforms appear to modulate cytoplasmic pathways switching cell fate towards cell survival or death. Main insights on this issue derive from some pathological conditions in which alterations of microdomains structure or function can lead to severe alterations of cell activity and life span. In the light of the role played by raft-like microdomains to integrate apoptotic signals and in regulating mitochondrial dynamics, it is conceivable that these membrane structures may play a role in the mitochondrial alterations observed in some of the most common human neurodegenerative diseases, such as Amyotrophic lateral sclerosis, Huntington's chorea and prion-related diseases. These findings introduce an additional task for identifying new molecular target(s) of pharmacological agents in these pathologies