Evolutionary Computation on Road Safety

This study examines the psychological research that focuses on road safety in Smart Cities as proposed by the Vulnerable Road Users (VRUs) sphere. It takes into account qualities such as VRUs’ personal information, their habits, environmental measurements and things data. With the goal of seeing VRUs as active and proactive actors with differentiated feelings and behaviours, we are committed to integrating the social factors that characterize each VRU into our social machinery. As a result, we will focus on the development of a VRU Social Machine to assess VRUs’ behaviour in order to improve road safety. The formal background will be to use Logic Programming to define its architecture based on a Deep Learning approach to Knowledge Representation and Reasoning, complemented with an Evolutionary approach to Computing

Fluid Dynamics in a Thrust Fault Inferred from Petrology and Geochemistry of Calcite Veins: An Example from the Southern Pyrenees

Petrographic and geochemical analyses (δ18O, δ13C, 87Sr/86Sr, clumped isotopes, and elemental composition) coupled with field structural data of synkinematic calcite veins, fault rocks, and host rocks are used to reconstruct the episodic evolution of an outstanding exposed thrust zone in the Southern Pyrenees and to evaluate the fault behavior as a conduit or barrier to fluid migration. The selected thrust displaces the steeply dipping southern limb of the Sant Corneli-Bóixols anticline, juxtaposing a Cenomanian-Turonian carbonate unit against a Coniacian carbonate sequence. Successive deformation events are recorded by distinct fracture systems and related calcite veins, highlighting (i) an episodic evolution of the thrust zone, resulting from an upward migration of the fault tip (process zone development) before growth of the fault (thrust slip plane propagation), and (ii) compartmentalization of the thrust fault zone, leading to different structural and fluid flow histories in the footwall and hanging wall. Fractures within the footwall comprise three systematically oriented fracture sets (F1, F2, and F3), each sealed by a separate generation calcite cement, and a randomly oriented fracture system (mosaic to chaotic breccia), cemented by the same cements as fracture sets F1 and F2. The formation of fractures F1 and F2 and the mosaic to chaotic breccia is consistent with dilatant fracturing within the process zone (around the fault tip) during initial fault growth, whereas the formation of the latest fracture system points to hybrid shear-dilational failure during propagation of the fault. The continuous formation of different fracture systems and related calcite cementation phases evidences that the structural permeability in the footwall was transient and that the fluid pathways and regime evolved due to successive events of fracture opening and calcite cementation. Clumped isotopes evidence a progressive increase in precipitation temperatures from around 50°C to 117°C approximately, interpreted as burial increase linked to thrust sheet emplacement. During this period, the source of fluid changed from meteoric fluids to evolved meteoric fluids due to the water-rock interaction at increasing depths and temperatures. Contrary to the footwall, within the hanging wall, only randomly oriented fractures are recognized and the resulting crackle proto-breccia is sealed by a later and different calcite cement, which is also observed in the main fault plane and in the fault core. This cement precipitated from formation fluids, at around 95°C, that circulated along the fault core and in the hanging wall block, again supporting the interpretation of compartmentalization of the thrust structure. The integration of these data reveals that the studied thrust fault acted as a transverse barrier, dividing the thrust zone into two separate fluid compartments, and a longitudinal drain for migration of fluids. This study also highlights the similarity in deformation processes and mechanisms linked to the evolution of fault zones in compressional and extensional regimes involving carbonate rocks

Recurrent De Novo NAHR Reciprocal Duplications in the ATAD3 Gene Cluster Cause a Neurogenetic Trait with Perturbed Cholesterol and Mitochondrial Metabolism.

Recent studies have identified both recessive and dominant forms of mitochondrial disease that result from ATAD3A variants. The recessive form includes subjects with biallelic deletions mediated by non-allelic homologous recombination. We report five unrelated neonates with a lethal metabolic disorder characterized by cardiomyopathy, corneal opacities, encephalopathy, hypotonia, and seizures in whom a monoallelic reciprocal duplication at the ATAD3 locus was identified. Analysis of the breakpoint junction fragment indicated that these 67 kb heterozygous duplications were likely mediated by non-allelic homologous recombination at regions of high sequence identity in ATAD3A exon 11 and ATAD3C exon 7. At the recombinant junction, the duplication allele produces a fusion gene derived from ATAD3A and ATAD3C, the protein product of which lacks key functional residues. Analysis of fibroblasts derived from two affected individuals shows that the fusion gene product is expressed and stable. These cells display perturbed cholesterol and mitochondrial DNA organization similar to that observed for individuals with severe ATAD3A deficiency. We hypothesize that the fusion protein acts through a dominant-negative mechanism to cause this fatal mitochondrial disorder. Our data delineate a molecular diagnosis for this disorder, extend the clinical spectrum associated with structural variation at the ATAD3 locus, and identify a third mutational mechanism for ATAD3 gene cluster variants. These results further affirm structural variant mutagenesis mechanisms in sporadic disease traits, emphasize the importance of copy number analysis in molecular genomic diagnosis, and highlight some of the challenges of detecting and interpreting clinically relevant rare gene rearrangements from next-generation sequencing data

Sleep disturbances in tension-type headache and migraine

Current research into the pathogenesis of tension-type headache (TTH) and migraine is focused on altered nociceptive pain processing. Among the potential factors that influence sensitization mechanisms, emotional stress, depression, or sleep disorders all have an essential role: they increase the excitability of nociceptive firing and trigger hyperalgesic responses. Sleep disturbances and headache disorders share common brain structures and pathogenic mechanisms and TTH, migraine, and sleep disturbances often occur together; for example, 50% of individuals who have either TTH or migraine have insomnia. Moreover, insomnia and poor sleep quality have been associated with a higher frequency and intensity of headache attacks, supporting the notion that severity and prevalence of sleep problems correlate with headache burden. It should be noted that the association between headaches and sleep problems is bidirectional: headache can promote sleep disturbances, and sleep disturbances can also precede or trigger a headache attack. Therefore, a better understanding of the factors that affect sleep quality in TTH and migraine can assist clinicians in determining better and adequate therapeutic programs. In this review, the role of sleep disturbances in headaches, and the association with depression, emotional stress, and pain sensitivity in individuals with TTH or migraine are discussed

Displacement of the Scholar? Participatory Action Research under COVID-19

The impact of COVID-19 on conducting research is far-reaching, especially for those scholars working for or alongside communities. As the pandemic continues to create and exacerbate many of the issues that communities at the margins faced pre-pandemic, such as health disparities and access to resources, it also creates particular difficulties in collaborative, co-developed participatory research and scholar-activism. These forms of community engagement require the commitment of researchers to look beyond the purview of the racialized capitalist and neoliberal structures and institutions that tend to limit the scope of our research and engagement. Both the presence of the researcher within the community as well as deep community trust in the researcher is required in order to identify and prioritize local, often counter-hegemonic forms of knowledge production, resources, and support networks. The pandemic and similar conditions of crises has likely limited opportunities for building long-term, productive relationships of mutual trust and reciprocity needed for PAR while communities refocus on meeting basic needs. The pandemic has now not only exacerbated existing disparities and made the need for engaged, critical and co-creative partnerships even greater, it has also abruptly halted opportunities for partnerships to occur, and further constrained funds to support communities partnering with researchers. In this paper we highlight accomplishments and discuss the many challenges that arise as participatory action researchers are displaced from the field and classroom, such as funding obstacles and working remotely. An analysis of experiences of the displacement of the scholar exposes the conflicts of conducting PAR during crises within a state of academic capitalism. These experiences are drawn from our work conducting PAR during COVID-19 around the globe, both in urban and rural settings, and during different stages of engagement. From these findings the case is made for mutual learning from peer-experiences and institutional support for PAR. As future crises are expected, increased digital resources and infrastructure, academic flexibility and greater consideration of PAR, increased funding for PAR, and dedicated institutional support programs for PAR are needed

Solar-type dynamo behaviour in fully convective stars without a tachocline

In solar-type stars (with radiative cores and convective envelopes), the magnetic field powers star spots, flares and other solar phenomena, as well as chromospheric and coronal emission at ultraviolet to X-ray wavelengths. The dynamo responsible for generating the field depends on the shearing of internal magnetic fields by differential rotation. The shearing has long been thought to take place in a boundary layer known as the tachocline between the radiative core and the convective envelope. Fully convective stars do not have a tachocline and their dynamo mechanism is expected to be very different, although its exact form and physical dependencies are not known. Here we report observations of four fully convective stars whose X-ray emission correlates with their rotation periods in the same way as in Sun-like stars. As the X-ray activity - rotation relationship is a well-established proxy for the behaviour of the magnetic dynamo, these results imply that fully convective stars also operate a solar-type dynamo. The lack of a tachocline in fully convective stars therefore suggests that this is not a critical ingredient in the solar dynamo and supports models in which the dynamo originates throughout the convection zone.Comment: 6 pages, 1 figure. Accepted for publication in Nature (28 July 2016). Author's version, including Method

Role of cellular senescence and NOX4-mediated oxidative stress in systemic sclerosis pathogenesis.

Systemic sclerosis (SSc) is a systemic autoimmune disease characterized by progressive fibrosis of skin and numerous internal organs and a severe fibroproliferative vasculopathy resulting frequently in severe disability and high mortality. Although the etiology of SSc is unknown and the detailed mechanisms responsible for the fibrotic process have not been fully elucidated, one important observation from a large US population study was the demonstration of a late onset of SSc with a peak incidence between 45 and 54 years of age in African-American females and between 65 and 74 years of age in white females. Although it is not appropriate to consider SSc as a disease of aging, the possibility that senescence changes in the cellular elements involved in its pathogenesis may play a role has not been thoroughly examined. The process of cellular senescence is extremely complex, and the mechanisms, molecular events, and signaling pathways involved have not been fully elucidated; however, there is strong evidence to support the concept that oxidative stress caused by the excessive generation of reactive oxygen species may be one important mechanism involved. On the other hand, numerous studies have implicated oxidative stress in SSc pathogenesis, thus, suggesting a plausible mechanism in which excessive oxidative stress induces cellular senescence and that the molecular events associated with this complex process play an important role in the fibrotic and fibroproliferative vasculopathy characteristic of SSc. Here, recent studies examining the role of cellular senescence and of oxidative stress in SSc pathogenesis will be reviewed

Protective role of DNJ-27/ERdj5 in Caenorhabditis elegans models of human neurodegenerative diseases

Aims: Cells have developed quality control systems for protection against proteotoxicity. Misfolded and aggregation-prone proteins, which are behind the initiation and progression of many neurodegenerative diseases (ND), are known to challenge the proteostasis network of the cells. We aimed to explore the role of DNJ-27/ERdj5, an endoplasmic reticulum (ER)-resident thioredoxin protein required as a disulfide reductase for the degradation of misfolded proteins, in well-established Caenorhabditis elegans models of Alzheimer, Parkinson and Huntington diseases. Results: We demonstrate that DNJ-27 is an ER luminal protein and that its expression is induced upon ER stress via IRE-1/XBP-1. When dnj-27 expression is downregulated by RNA interference we find an increase in the aggregation and associated pathological phenotypes (paralysis and motility impairment) caused by human β-amyloid peptide (Aβ), α-synuclein (α-syn) and polyglutamine (polyQ) proteins. In turn, DNJ-27 overexpression ameliorates these deleterious phenotypes. Surprisingly, despite being an ER-resident protein, we show that dnj-27 downregulation alters cytoplasmic protein homeostasis and causes mitochondrial fragmentation. We further demonstrate that DNJ-27 overexpression substantially protects against the mitochondrial fragmentation caused by human Aβ and α-syn peptides in these worm models. Innovation: We identify C. elegans dnj-27 as a novel protective gene for the toxicity associated with the expression of human Aβ, α-syn and polyQ proteins, implying a protective role of ERdj5 in Alzheimer, Parkinson and Huntington diseases. Conclusion: Our data support a scenario where the levels of DNJ-27/ERdj5 in the ER impact cytoplasmic protein homeostasis and the integrity of the mitochondrial network which might underlie its protective effects in models of proteotoxicity associated to human ND