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Successive locations of individual large earthquakes ( M w  > 5.5) over years to centuries can be difficult to explain with simple Coulomb stress transfer (CST) because it is common for seismicity to circumvent nearest-neighbour along-strike faults where coseismic CST is greatest. We demonstrate that Coulomb pre-stress (the cumulative CST from multiple earthquakes and interseismic loading on non-planar faults) may explain this, evidenced by study of a 667-year historical record of earthquakes in central Italy. Heterogeneity in Coulomb pre-stresses across the fault system is >±50 bars, whereas coseismic CST is <±2 bars, so the latter will rarely overwhelm the former, explaining why historical earthquakes rarely rupture nearest neighbor faults. However, earthquakes do tend to occur where the cumulative coseismic and interseismic CST is positive, although there are notable examples where earthquake propagate across negatively stressed portions of faults. Hence Coulomb pre-stress calculated for non-planar faults is an ignored yet vital factor for earthquake triggering. Scattered earthquake locations in the same region cannot be explained solely by coseismic Coulomb stress on planar faults. Instead, the authors suggest Coulomb pre-stress to influence earthquake locations. Pre-stress was modelled on strike-variable faults and consists of coseismic and interseismic Coulomb stress.

Surface faulting earthquakes are known to cluster in time from historical and palaeoseismic studies, but the mechanism(s) responsible for clustering, such as fault interaction, strain-storage, and evolving dynamic topography, are poorly quantified, and hence not well understood. We present a quantified replication of observed earthquake clustering in central Italy. Six active normal faults are studied using 36 Cl cosmogenic dating, revealing out-of-phase periods of high or low surface slip-rate on neighboring structures that we interpret as earthquake clusters and anticlusters. Our calculations link stress transfer caused by slip averaged over clusters and anti-clusters on coupled fault/shear-zone structures to viscous flow laws. We show that (1) differential stress fluctuates during fault/shear-zone interactions, and (2) these fluctuations are of sufficient magnitude to produce changes in strain-rate on viscous shear zones that explain slip-rate changes on their overlying brittle faults. These results suggest that fault/shear-zone interactions are a plausible explanation for clustering, opening the path towards process-led seismic hazard assessments. The mechanisms responsible for clustering of surface fault earthquakes are often unclear. Here the authors find that differential stress fluctuates during fault/shear-zone interactions which can produce changes in strain-rate and slip-rate changes leading to earthquake clustering.

The 28th December 1908 Messina earthquake (Mw 7.1), Italy, caused >80,000 deaths and transformed earthquake science by triggering the study of earthquake environmental effects worldwide, yet its source is still a matter of debate. To constrain the geometry and kinematics of the earthquake we use elastic half-space modelling on non-planar faults, constrained by the geology and geomorphology of the Messina Strait, to replicate levelling data from 1907–1909. The novelty of our approach is that we (a) recognise the similarity between the pattern of vertical motions and that of other normal faulting earthquakes, and (b) for the first time model the levelling data using the location and geometry of a well-known offshore capable fault. Our results indicate slip on the capable fault with a dip to the east of 70° and 5 m dip-slip at depth, with slip propagating to the surface on the sea bed. Our work emphasises that geological and geomorphological observations supporting maps of capable non-planar faults should not be ignored when attempting to identify the sources of major earthquakes.

Individuality is a striking feature of animal behavior. Individual animals differ in traits and preferences which shape their interactions and their prospects for survival. However, the mechanisms underlying behavioral individuation are poorly understood and are generally considered to be genetic-based. Here, we devised a large environment, Souris City, in which mice live continuously in large groups. We observed the emergence of individual differences in social behavior, activity levels, and cognitive traits, even though the animals had low genetic diversity (inbred C57BL/6J strain). We further show that the phenotypic divergence in individual behaviors was mirrored by developing differences in midbrain dopamine neuron firing properties. Strikingly, modifying the social environment resulted in a fast re-adaptation of both the animal’s traits and its dopamine firing pattern. Individuality can rapidly change upon social challenges, and does not just depend on the genetic status or the accumulation of small differences throughout development. Individual animals differ in behavioral traits, but the mechanisms underlying individuation are unclear. Here, the authors show that mice living in a ‘city’ develop individual behavior differences, associated with changes in dopamine cell firing, that can be reversed on moving them to a different social environment.

Imbibition in poplar wood is studied from macroscopic measurements (mass and deformation) along with magnetic resonance imaging experiments allowing to observe bound and free water dynamics. Additional experiments with silicone oil allow to compare the characteristics of water imbibition with those of a liquid not hygroscopically adsorbed in wood. It was shown that, in contrast to porous media with an impermeable solid structure, the water imbibition in the hydraulic conduits of hardwood is not simply driven by the standard capillary effects associated with a good wetting of the solid surface, but it is in fact strongly affected by the adsorption of bound water in cell walls. More precisely bound water appears to progress far beyond the front of free water, and the free water penetration along the sample axis apparently coincides with the development of a region saturated with bound water. This likely explains that water imbibition is about three orders of magnitude slower than expected from standard Washburn imbibition process.

Epidemiological studies report strong association between mood disorders and tobacco addiction. This high comorbidity requires adequate treatment but the underlying mechanisms are unknown. We demonstrate that nicotine exposure, independent of drug withdrawal effects, increases stress sensitivity, a major risk factor in mood disorders. Nicotine and stress concur to induce long-lasting cellular adaptations within the dopamine (DA) system. This interplay is underpinned by marked remodeling of nicotinic systems, causing increased ventral tegmental area (VTA) DA neurons’ activity and stress-related behaviors, such as social aversion. Blocking β2 or α7 nicotinic acetylcholine receptors (nAChRs) prevents, respectively, the development and the expression of social stress-induced neuroadaptations; conversely, facilitating α7 nAChRs activation specifically in the VTA promotes stress-induced cellular and behavioral maladaptations. Our work unravels a complex nicotine-stress bidirectional interplay and identifies α7 nAChRs as a promising therapeutic target for stress-related psychiatric disorders.

The two sides of nicotine The bad news, nicotine addiction has caused the deaths of millions from smoking-related diseases. The good news, nicotine can enhance cognitive performance. In an attempt to disentangle the brain networks that mediate nicotine reward and relevant cognitive functions, Maskos et al . have developed an injectable lentiviral vector that delivers functional nicotinic acetylcholine receptors to defined regions of the mouse brain. The technique was used to generate mice that express nicotinic receptors exclusively in the midbrain ventral tegmental area, the VTA, which contains dopamine reward neurons and is associated with the response to drugs of abuse. The experiment showed that these receptors in the VTA are sufficient for all behavioural and physiological phenomena associated with nicotine dependence. And they are also involved in the higher brain or ‘cognitive’ functions in the mouse. Nicotine's ‘good’ and ‘bad’ sides are, it seems, intimately entangled and originate from a phylogenetically ancient part of the brain. Worldwide, 100 million people are expected to die this century from the consequences of nicotine addiction 1 , but nicotine is also known to enhance cognitive performance 2 . Identifying the molecular mechanisms involved in nicotine reinforcement and cognition is a priority and requires the development of new in vivo experimental paradigms. The ventral tegmental area (VTA) of the midbrain is thought to mediate the reinforcement properties of many drugs of abuse. Here we specifically re-expressed the β2-subunit of the nicotinic acetylcholine receptor (nAChR) by stereotaxically injecting a lentiviral vector into the VTA of mice carrying β2-subunit deletions 3 , 4 . We demonstrate the efficient re-expression of electrophysiologically responsive, ligand-binding nicotinic acetylcholine receptors in dopamine-containing neurons of the VTA, together with the recovery of nicotine-elicited dopamine release and nicotine self-administration. We also quantified exploratory behaviours of the mice, and showed that β2-subunit re-expression restored slow exploratory behaviour (a measure of cognitive function) to wild-type levels, but did not affect fast navigation behaviour. We thus demonstrate the sufficient role of the VTA in both nicotine reinforcement and endogenous cholinergic regulation of cognitive functions.

The flow of ductile rocks in the deep crust and uppermost mantle is thought to add stress to faults in the shallow crust, potentially bringing the faults closer to rupture. Measurements of fault offsets in the Italian Apennines show that earthquake recurrence is largely controlled by viscous flow of deeper rocks in localized zones. Viscous flow in the deep crust and uppermost mantle can contribute to the accumulation of strain along seismogenic faults in the shallower crust 1 . It is difficult to evaluate this contribution to fault loading because it is unclear whether the viscous deformation occurs in localized shear zones or is more broadly distributed 2 . Furthermore, the rate of strain accumulation by viscous flow has a power law dependence on the stress applied, yet there are few direct estimates of what the power law exponent is, over the long term, for active faults. Here we measure topography and the offset along fault surfaces created during successive episodes of slip on seismically active extensional faults in the Italian Apennines during the Holocene epoch. We show that these data can be used to derive a relationship between the stress driving deformation and the fault strain rate, averaged over about 15 thousand years (kyr). We find that this relationship follows a well-defined power law with an exponent in the range of 3.0–3.3 (1 σ ). This exponent is consistent with nonlinear viscous deformation in the deep crust and, crucially, strain localization promoted by seismogenic faulting at shallower depths. Although we cannot rule out some distributed deformation, we suggest that fault strain and thus earthquake recurrence in the Apennines is largely controlled by viscous flow in deep, localized shear zones, over many earthquake cycles.

Smoking is the most important preventable cause of morbidity and mortality worldwide. Recent genome-wide association studies highlighted a human haplotype on chromosome 15 underlying the risk for tobacco dependence and lung cancer. Several polymorphisms in the CHRNA3-CHRNA5-CHRNB4 cluster coding for the nicotinic acetylcholine receptor (nAChR) α3, α5 and β4 subunits were implicated. In mouse models, we define a key role in the control of sensitivity to nicotine for the α5 subunit in dopaminergic (DAergic) neurons of the ventral tegmental area (VTA). We first investigated the reinforcing effects of nicotine in drug-naive α5 −/− mice using an acute intravenous nicotine self-administration task and ex vivo and in vivo electrophysiological recordings of nicotine-elicited DA cell activation. We designed lentiviral re-expression vectors to achieve targeted re-expression of wild-type or mutant α5 in the VTA, in general, or in DA neurons exclusively. Our results establish a crucial role for α5*-nAChRs in DAergic neurons. These receptors are key regulators that determine the minimum nicotine dose necessary for DA cell activation and thus nicotine reinforcement. Finally, we demonstrate that a single-nucleotide polymorphism, the non-synonymous α5 variant rs16969968, frequent in many human populations, exhibits a partial loss of function of the protein in vivo . This leads to increased nicotine consumption in the self-administration paradigm. We thus define a critical link between a human predisposition marker, its expression in DA neurons and nicotine intake.

This is the premier study designed to evaluate the impact of thermal pre-treatment on the availability of polycyclic aromatic hydrocarbons (PAHs) for successive removal by chemical oxidation. Experiments were conducted in two soils having different PAH distribution originating from former coking plant sites (Homécourt, H, and Neuves Maisons, NM) located in northeast of France. Soil samples were pre-heated at 60, 100, and 150 °C for 1 week under inert atmosphere (N₂). Pre-heating resulted in slight removal of PAHs (<10 %) and loss of extractable organic matter (EOM). Then, these pre-heated soil samples were subjected to Fenton-like oxidation (H₂O₂ and magnetite) at room temperature. Chemical oxidation in soil without any pre-treatment showed almost no PAH degradation underscoring the unavailability of PAHs. However, chemical oxidation in pre-heated soils showed significant PAH degradation (19, 29, and 43 % in NM soil and 31, 36, and 47 % in H soil pre-treated at 60, 100, and 150 °C, respectively). No preferential removal of PAHs was observed after chemical oxidation in both soils. These results indicated the significant impact of pre-heating temperature on the availability of PAHs in contaminated soils and therefore may have strong implications in the remediation of contaminated soils especially where pollutant availability is a limiting factor.