Coseismic throw variation across along-strike bends on active normal faults: implications for displacement versus length scaling of earthquake ruptures

Fault bends, and associated changes in fault dip, play a key role in explaining the scatter in maximum offset versus surface rupture length fault scaling relationships. Detailed field measurements of the fault geometry and magnitude of slip in the 2016-2017 central Italy earthquake sequence, alongside three examples from large historical normal-faulting earthquakes in different tectonic settings, provide multiple examples in which coseismic throw increases across bends in fault strike where dip also increases beyond what is necessary to accommodate a uniform slip vector. Coseismic surface ruptures produced by two mainshocks of the 2016-2017 central Italy earthquake sequence (24th August 2016 Mw 6.0, 30th October 2016 Mw 6.5) cross a ~0.83 km amplitude along-strike bend, and the coseismic throws for both earthquakes increase by a factor of 2-3 where the strike of the fault changes by ~30o and the dip increases by 20-25o. We present similar examples from historical normal faulting earthquakes (1887, Sonora earthquake, Mw 7.5; 1981, Corinth earthquakes, Mw 6.7-6.4;1983, Borah Peak earthquake, Mw 7.3). We demonstrate that it is possible to estimate the expected change in throw across a bend by applying equations that relate strike, dip and slip vector to horizontal strain conservation along a non-planar fault for a single earthquake rupture. The calculated slip enhancement in bends can explain the scatter in maximum displacement (Dmax) versus surface rupture length scaling relationships. If fault bends are un-recognized, they can introduce variation in Dmax that may lead to erroneous inferences of stress drop variability for earthquakes, and maximum earthquake magnitudes derived from vertical offsets in paleoseismic datasets

Coseismic throw variation across along-strike bends on active normal faults: implications for displacement versus length scaling of earthquake ruptures

Fault bends, and associated changes in fault dip, play a key role in explaining the scatter in maximum offset versus surface rupture length fault scaling relationships. Detailed field measurements of the fault geometry and magnitude of slip in the 2016-2017 central Italy earthquake sequence, alongside three examples from large historical normal-faulting earthquakes in different tectonic settings, provide multiple examples in which coseismic throw increases across bends in fault strike where dip also increases beyond what is necessary to accommodate a uniform slip vector. Coseismic surface ruptures produced by two mainshocks of the 2016-2017 central Italy earthquake sequence (24th August 2016 Mw 6.0, 30th October 2016 Mw 6.5) cross a ~0.83 km amplitude along-strike bend, and the coseismic throws for both earthquakes increase by a factor of 2-3 where the strike of the fault changes by ~30o and the dip increases by 20-25o. We present similar examples from historical normal faulting earthquakes (1887, Sonora earthquake, Mw 7.5; 1981, Corinth earthquakes, Mw 6.7-6.4;1983, Borah Peak earthquake, Mw 7.3). We demonstrate that it is possible to estimate the expected change in throw across a bend by applying equations that relate strike, dip and slip vector to horizontal strain conservation along a non-planar fault for a single earthquake rupture. The calculated slip enhancement in bends can explain the scatter in maximum displacement (Dmax) versus surface rupture length scaling relationships. If fault bends are un-recognized, they can introduce variation in Dmax that may lead to erroneous inferences of stress drop variability for earthquakes, and maximum earthquake magnitudes derived from vertical offsets in paleoseismic datasets

Dual control of fault intersections on stop-start rupture in the 2016 Central Italy seismic sequence

Large continental earthquakes necessarily involve failure of multiple faults or segments. But these same critically-stressed systems sometimes fail in drawn-out sequences of smaller earthquakes over days or years instead. These two modes of failure have vastly different implications for seismic hazard and it is not known why fault systems sometimes fail in one mode or the other, or what controls the termination and reinitiation of slip in protracted seismic sequences. A paucity of modern observations of seismic sequences has hampered our understanding to-date, but a series of three Mw>6 earthquakes from August to November 2016 in Central Italy represents a uniquely well-observed example. Here we exploit a wealth of geodetic, seismological and field data to understand the spatio-temporal evolution of the sequence. Our results suggest that pre-existing fault structures controlled the extent and termination of rupture in each event in the sequence, and that fluid diffusion, channelled along these same structures, may have also determined the timing of rupture reinitiation. This dual control of subsurface structure on the stop-start rupture in seismic sequences may be common; future efforts should focus on investigating its prevalence

Impact of Simian Immunodeficiency Virus Infection on Chimpanzee Population Dynamics

Like human immunodeficiency virus type 1 (HIV-1), simian immunodeficiency virus of chimpanzees (SIVcpz) can cause CD4+ T cell loss and premature death. Here, we used molecular surveillance tools and mathematical modeling to estimate the impact of SIVcpz infection on chimpanzee population dynamics. Habituated (Mitumba and Kasekela) and non-habituated (Kalande) chimpanzees were studied in Gombe National Park, Tanzania. Ape population sizes were determined from demographic records (Mitumba and Kasekela) or individual sightings and genotyping (Kalande), while SIVcpz prevalence rates were monitored using non-invasive methods. Between 2002–2009, the Mitumba and Kasekela communities experienced mean annual growth rates of 1.9% and 2.4%, respectively, while Kalande chimpanzees suffered a significant decline, with a mean growth rate of −6.5% to −7.4%, depending on population estimates. A rapid decline in Kalande was first noted in the 1990s and originally attributed to poaching and reduced food sources. However, between 2002–2009, we found a mean SIVcpz prevalence in Kalande of 46.1%, which was almost four times higher than the prevalence in Mitumba (12.7%) and Kasekela (12.1%). To explore whether SIVcpz contributed to the Kalande decline, we used empirically determined SIVcpz transmission probabilities as well as chimpanzee mortality, mating and migration data to model the effect of viral pathogenicity on chimpanzee population growth. Deterministic calculations indicated that a prevalence of greater than 3.4% would result in negative growth and eventual population extinction, even using conservative mortality estimates. However, stochastic models revealed that in representative populations, SIVcpz, and not its host species, frequently went extinct. High SIVcpz transmission probability and excess mortality reduced population persistence, while intercommunity migration often rescued infected communities, even when immigrating females had a chance of being SIVcpz infected. Together, these results suggest that the decline of the Kalande community was caused, at least in part, by high levels of SIVcpz infection. However, population extinction is not an inevitable consequence of SIVcpz infection, but depends on additional variables, such as migration, that promote survival. These findings are consistent with the uneven distribution of SIVcpz throughout central Africa and explain how chimpanzees in Gombe and elsewhere can be at equipoise with this pathogen

New genetic loci link adipose and insulin biology to body fat distribution.

Body fat distribution is a heritable trait and a well-established predictor of adverse metabolic outcomes, independent of overall adiposity. To increase our understanding of the genetic basis of body fat distribution and its molecular links to cardiometabolic traits, here we conduct genome-wide association meta-analyses of traits related to waist and hip circumferences in up to 224,459 individuals. We identify 49 loci (33 new) associated with waist-to-hip ratio adjusted for body mass index (BMI), and an additional 19 loci newly associated with related waist and hip circumference measures (P < 5 × 10(-8)). In total, 20 of the 49 waist-to-hip ratio adjusted for BMI loci show significant sexual dimorphism, 19 of which display a stronger effect in women. The identified loci were enriched for genes expressed in adipose tissue and for putative regulatory elements in adipocytes. Pathway analyses implicated adipogenesis, angiogenesis, transcriptional regulation and insulin resistance as processes affecting fat distribution, providing insight into potential pathophysiological mechanisms

Causal effect of plasminogen activator inhibitor type 1 on coronary heart disease

Background--Plasminogen activator inhibitor type 1 (PAI-1) plays an essential role in the fibrinolysis system and thrombosis. Population studies have reported that blood PAI-1 levels are associated with increased risk of coronary heart disease (CHD). However, it is unclear whether the association reflects a causal influence of PAI-1 on CHD risk. Methods and Results--To evaluate the association between PAI-1 and CHD, we applied a 3-step strategy. First, we investigated the observational association between PAI-1 and CHD incidence using a systematic review based on a literature search for PAI-1 and CHD studies. Second, we explored the causal association between PAI-1 and CHD using a Mendelian randomization approach using summary statistics from large genome-wide association studies. Finally, we explored the causal effect of PAI-1 on cardiovascular risk factors including metabolic and subclinical atherosclerosis measures. In the systematic meta-analysis, the highest quantile of blood PAI-1 level was associated with higher CHD risk comparing with the lowest quantile (odds ratio=2.17; 95% CI: 1.53, 3.07) in an age- and sex-adjusted model. The effect size was reduced in studies using a multivariable-adjusted model (odds ratio=1.46; 95% CI: 1.13, 1.88). The Mendelian randomization analyses suggested a causal effect of increased PAI-1 level on CHD risk (odds ratio=1.22 per unit increase of log-transformed PAI-1; 95% CI: 1.01, 1.47). In addition, we also detected a causal effect of PAI-1 on elevating blood glucose and high-density lipoprotein cholesterol. Conclusions--Our study indicates a causal effect of elevated PAI-1 level on CHD risk, which may be mediated by glucose dysfunction

Molecular mechanisms of cell death: recommendations of the Nomenclature Committee on Cell Death 2018.

Over the past decade, the Nomenclature Committee on Cell Death (NCCD) has formulated guidelines for the definition and interpretation of cell death from morphological, biochemical, and functional perspectives. Since the field continues to expand and novel mechanisms that orchestrate multiple cell death pathways are unveiled, we propose an updated classification of cell death subroutines focusing on mechanistic and essential (as opposed to correlative and dispensable) aspects of the process. As we provide molecularly oriented definitions of terms including intrinsic apoptosis, extrinsic apoptosis, mitochondrial permeability transition (MPT)-driven necrosis, necroptosis, ferroptosis, pyroptosis, parthanatos, entotic cell death, NETotic cell death, lysosome-dependent cell death, autophagy-dependent cell death, immunogenic cell death, cellular senescence, and mitotic catastrophe, we discuss the utility of neologisms that refer to highly specialized instances of these processes. The mission of the NCCD is to provide a widely accepted nomenclature on cell death in support of the continued development of the field