Transient landscapes at fault tips

Fault growth produces patterns of displacement and slip rate that are highly variable in both space and time. This transience is most pronounced near fault tips, where along‐strike displacement gradients vary in time as the fault array lengthens. We use a set of statistical and field observations to quantify the response of catchments and their associated fans in three large normal fault arrays to transient patterns of displacement and slip rate. Catchments near the fault tips show distinct scaling of channel slope with drainage area compared with catchments near the strike center. This scaling becomes uniform beyond about ∼10 km from the fault tips and is therefore like footwall relief, largely decoupled from the fault displacement profile. The estimated catchment response times to a change in slip rate also vary between fault tips and strike center. The response times for tip catchments are much longer than the inferred time since fault activity began, indicating that they are unlikely to be in equilibrium with the current fault displacement field. This disequilibrium, combined with the decoupling of slope‐area scaling from displacement, indicates that landscapes are most sensitive to fault activity near fault tips. Active faults characterized by along‐strike variation in slip rate thus provide excellent opportunities to explore the transient response of landscapes to tectonic forcing

Landscape evolution at extensional relay zones

It is commonly argued that the extensional relay zones between adjacent crustal-scale normal fault segments are associated with large catchment-fan systems that deliver significant amounts of sediment to hanging wall basins. This conceptual model of extensional basin development, while useful, overlooks some of the physical constraints on catchment evolution and sediment supply in relay zones. We argue that a key factor in the geomorphic evolution of relay zones is the interplay between two different timescales, the time over which the fault array develops, and the time over which the footwall catchment-fan systems are established. Results of numerical experiments using a landscape evolution model suggest that, in isolated fault blocks, footwall catchment evolution is highly dependent on the pattern and rate of fault array growth. A rapidly linked en echelon fault geometry gives rise to capture of relay zone drainage by aggressive catchment incision in the relay zone and to consequent increases in the rate of sediment supply to the hanging wall. Capture events do not occur when the fault segments are allowed to propagate slowly toward an en echelon geometry. In neither case, however, are large relay zone catchment-fan systems developed. We propose several physical reasons for this, including geometric constraints and limits on catchment incision and sediment transport rates in relay zones. Future research efforts should focus on the timescales over which fault array development occurs, and on the quantitative variations in catchment-fan system morphology at relay zones

DCC Dynamics in (2+1)D-O(3) model

The dynamics of symmetry-breaking after a quench is numerically simulated on a lattice for the (2+1)-dimensional O(3) model. In addition to the standard sigma-model with temperature-dependent Phi^4-potential the energy functional includes a four-derivative current-current coupling to stabilize the size of the emerging extended topological textures. The total winding number can be conserved by constraint. As a model for the chiral phase transition during the cooling phase after a hadronic collision this allows to investigate the interference of 'baryon-antibaryon' production with the developing disoriented aligned domains. The growth of angular correlations, condensate, average orientation is studied in dependence of texture size, quench rate, symmetry breaking. The classical dissipative dynamics determines the rate of energy emitted from the relaxing source for each component of the 3-vector field which provides a possible signature for domains of Disoriented Chiral Condensate. We find that the 'pions' are emitted in two distinct pulses; for sufficiently small lattice size the second one carries the DCC signal, but it is strongly suppressed as compared to simultaneous 'sigma'-meson emission. We compare the resulting anomalies in the distributions of DCC pions with probabilities derived within the commonly used coherent state formalism.Comment: 27 pages, 17 figures; several minor insertions in the text; two references adde

Multicomponent theory of buoyancy instabilities in magnetized plasmas: The case of magnetic field parallel to gravity

We investigate electromagnetic buoyancy instabilities of the electron-ion plasma with the heat flux based on not the magnetohydrodynamic (MHD) equations, but using the multicomponent plasma approach when the momentum equations are solved for each species. We consider a geometry in which the background magnetic field, gravity, and stratification are directed along one axis. The nonzero background electron thermal flux is taken into account. Collisions between electrons and ions are included in the momentum equations. No simplifications usual for the one-fluid MHD-approach in studying these instabilities are used. We derive a simple dispersion relation, which shows that the thermal flux perturbation generally stabilizes an instability for the geometry under consideration. This result contradicts to conclusion obtained in the MHD-approach. We show that the reason of this contradiction is the simplified assumptions used in the MHD analysis of buoyancy instabilities and the role of the longitudinal electric field perturbation which is not captured by the ideal MHD equations. Our dispersion relation also shows that the medium with the electron thermal flux can be unstable, if the temperature gradients of ions and electrons have the opposite signs. The results obtained can be applied to the weakly collisional magnetized plasma objects in laboratory and astrophysics.Comment: Accepted for publication in Astrophysics & Space Scienc

Insights into malaria susceptibility using genome-wide data on 17,000 individuals from Africa, Asia and Oceania

The human genetic factors that affect resistance to infectious disease are poorly understood. Here we report a genome-wide association study in 17,000 severe malaria cases and population controls from 11 countries, informed by sequencing of family trios and by direct typing of candidate loci in an additional 15,000 samples. We identify five replicable associations with genome-wide levels of evidence including a newly implicated variant on chromosome 6. Jointly, these variants account for around one-tenth of the heritability of severe malaria, which we estimate as -23% using genome-wide genotypes. We interrogate available functional data and discover an erythroid-specific transcription start site underlying the known association in ATP2B4, but are unable to identify a likely causal mechanism at the chromosome 6 locus. Previously reported HLA associations do not replicate in these samples. This large dataset will provide a foundation for further research on thegenetic determinants of malaria resistance in diverse populations.Peer reviewe

The global, regional, and national burden of pancreatic cancer and its attributable risk factors in 195 countries and territories, 1990-2017: a systematic analysis for the Global Burden of Disease Study 2017

Background: Worldwide, both the incidence and death rates of pancreatic cancer are increasing. Evaluation of pancreatic cancer burden and its global, regional, and national patterns is crucial to policy making and better resource allocation for controlling pancreatic cancer risk factors, developing early detection methods, and providing faster and more effective treatments. Methods: Vital registration, vital registration sample, and cancer registry data were used to generate mortality, incidence, and disability-adjusted life-years (DALYs) estimates. We used the comparative risk assessment framework to estimate the proportion of deaths attributable to risk factors for pancreatic cancer: smoking, high fasting plasma glucose, and high body-mass index. All of the estimates were reported as counts and age-standardised rates per 100 000 person-years. 95% uncertainty intervals (UIs) were reported for all estimates. Findings: In 2017, there were 448 000 (95% UI 439 000\u2013456 000) incident cases of pancreatic cancer globally, of which 232 000 (210 000\u2013221 000; 51\ub79%) were in males. The age-standardised incidence rate was 5\ub70 (4\ub79\u20135\ub71) per 100 000 person-years in 1990 and increased to 5\ub77 (5\ub76\u20135\ub78) per 100 000 person-years in 2017. There was a 2\ub73 times increase in number of deaths for both sexes from 196 000 (193 000\u2013200 000) in 1990 to 441 000 (433 000\u2013449 000) in 2017. There was a 2\ub71 times increase in DALYs due to pancreatic cancer, increasing from 4\ub74 million (4\ub73\u20134\ub75) in 1990 to 9\ub71 million (8\ub79\u20139\ub73) in 2017. The age-standardised death rate of pancreatic cancer was highest in the high-income super-region across all years from 1990 to 2017. In 2017, the highest age-standardised death rates were observed in Greenland (17\ub74 [15\ub78\u201319\ub70] per 100 000 person-years) and Uruguay (12\ub71 [10\ub79\u201313\ub75] per 100 000 person-years). These countries also had the highest age-standardised death rates in 1990. Bangladesh (1\ub79 [1\ub75\u20132\ub73] per 100 000 person-years) had the lowest rate in 2017, and S\ue3o Tom\ue9 and Pr\uedncipe (1\ub73 [1\ub71\u20131\ub75] per 100 000 person-years) had the lowest rate in 1990. The numbers of incident cases and deaths peaked at the ages of 65\u201369 years for males and at 75\u201379 years for females. Age-standardised pancreatic cancer deaths worldwide were primarily attributable to smoking (21\ub71% [18\ub78\u201323\ub77]), high fasting plasma glucose (8\ub79% [2\ub71\u201319\ub74]), and high body-mass index (6\ub72% [2\ub75\u201311\ub74]) in 2017. Interpretation: Globally, the number of deaths, incident cases, and DALYs caused by pancreatic cancer has more than doubled from 1990 to 2017. The increase in incidence of pancreatic cancer is likely to continue as the population ages. Prevention strategies should focus on modifiable risk factors. Development of screening programmes for early detection and more effective treatment strategies for pancreatic cancer are needed. Funding: Bill & Melinda Gates Foundation

Histone H3.3 beyond cancer: Germline mutations in Histone 3 Family 3A and 3B cause a previously unidentified neurodegenerative disorder in 46 patients

Although somatic mutations in Histone 3.3 (H3.3) are well-studied drivers of oncogenesis, the role of germline mutations remains unreported. We analyze 46 patients bearing de novo germline mutations in histone 3 family 3A (H3F3A) or H3F3B with progressive neurologic dysfunction and congenital anomalies without malignancies. Molecular modeling of all 37 variants demonstrated clear disruptions in interactions with DNA, other histones, and histone chaperone proteins. Patient histone posttranslational modifications (PTMs) analysis revealed notably aberrant local PTM patterns distinct from the somatic lysine mutations that cause global PTM dysregulation. RNA sequencing on patient cells demonstrated up-regulated gene expression related to mitosis and cell division, and cellular assays confirmed an increased proliferative capacity. A zebrafish model showed craniofacial anomalies and a defect in Foxd3-derived glia. These data suggest that the mechanism of germline mutations are distinct from cancer-associated somatic histone mutations but may converge on control of cell proliferation