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The propensity for dynamic earthquake triggering is thought to depend on the local stress state and amplitude of the stress perturbation. However, the nature of this dependency has not been confirmed within a single crustal volume. Here, we show that at Sierra Negra volcano, Galápagos Islands, the intensity of dynamically triggered earthquakes increased as inflation of a magma reservoir elevated the stress state. The perturbation of short-term seismicity within teleseismic surface waves also increased with peak dynamic strain. Following rapid coeruptive subsidence and reduction in stress and background seismicity rates, equivalent dynamic strains no longer triggered detectable seismicity. These findings offer direct constraints on the primary controls on dynamic triggering and suggest that the response to dynamic stresses may help constrain the evolution of volcanic unrest.

Recent large basaltic eruptions began after only minor surface uplift and seismicity, and resulted in caldera subsidence. In contrast, some eruptions at Galápagos Island volcanoes are preceded by prolonged, large amplitude uplift and elevated seismicity. These systems also display long-term intra-caldera uplift, or resurgence. However, a scarcity of observations has obscured the mechanisms underpinning such behaviour. Here we combine a unique multiparametric dataset to show how the 2018 eruption of Sierra Negra contributed to caldera resurgence. Magma supply to a shallow reservoir drove 6.5 m of pre-eruptive uplift and seismicity over thirteen years, including an Mw5.4 earthquake that triggered the eruption. Although co-eruptive magma withdrawal resulted in 8.5 m of subsidence, net uplift of the inner-caldera on a trapdoor fault resulted in 1.5 m of permanent resurgence. These observations reveal the importance of intra-caldera faulting in affecting resurgence, and the mechanisms of eruption in the absence of well-developed rift systems.

Human activity causes vibrations that propagate into the ground as high-frequency seismic waves. Measures to mitigate the coronavirus disease 2019 (COVID-19) pandemic caused widespread changes in human activity, leading to a months-long reduction in seismic noise of up to 50%. The 2020 seismic noise quiet period is the longest and most prominent global anthropogenic seismic noise reduction on record. Although the reduction is strongest at surface seismometers in populated areas, this seismic quiescence extends for many kilometers radially and hundreds of meters in depth. This quiet period provides an opportunity to detect subtle signals from subsurface seismic sources that would have been concealed in noisier times and to benchmark sources of anthropogenic noise. A strong correlation between seismic noise and independent measurements of human mobility suggests that seismology provides an absolute, real-time estimate of human activities., (Copyright © 2020 The Authors, some rights reserved; exclusive licensee American Association for the Advancement of Science. No claim to original U.S. Government Works.)

Crust at many divergent plate boundaries forms primarily by the injection of vertical sheet-like dykes, some tens of kilometres long. Previous models of rifting events indicate either lateral dyke growth away from a feeding source, with propagation rates decreasing as the dyke lengthens, or magma flowing vertically into dykes from an underlying source, with the role of topography on the evolution of lateral dykes not clear. Here we show how a recent segmented dyke intrusion in the Bárðarbunga volcanic system grew laterally for more than 45 kilometres at a variable rate, with topography influencing the direction of propagation. Barriers at the ends of each segment were overcome by the build-up of pressure in the dyke end; then a new segment formed and dyke lengthening temporarily peaked. The dyke evolution, which occurred primarily over 14 days, was revealed by propagating seismicity, ground deformation mapped by Global Positioning System (GPS), interferometric analysis of satellite radar images (InSAR), and graben formation. The strike of the dyke segments varies from an initially radial direction away from the Bárðarbunga caldera, towards alignment with that expected from regional stress at the distal end. A model minimizing the combined strain and gravitational potential energy explains the propagation path. Dyke opening and seismicity focused at the most distal segment at any given time, and were simultaneous with magma source deflation and slow collapse at the Bárðarbunga caldera, accompanied by a series of magnitude M > 5 earthquakes. Dyke growth was slowed down by an effusive fissure eruption near the end of the dyke. Lateral dyke growth with segment barrier breaking by pressure build-up in the dyke distal end explains how focused upwelling of magma under central volcanoes is effectively redistributed over long distances to create new upper crust at divergent plate boundaries.

Staphylococcal enterotoxins SEB and SEC3 and toxic shock syndrome toxin TSST-1 act as superantigens by overstimulating the human immune system and thereby compromise host defense. The mechanism of pathogenesis is explained on the basis of superantigen binding to the MHC class II receptor on the antigen presenting cell and to the T cell receptor (TcR) on the T cell. SEB, SEC3 and TSST-1 bind as intact proteins and make contacts with the alpha1 subdomain (DRalpha) of MHC class II and Vbeta subdomain of TcR. SEB, SEC3 and TSST-1 show specificities for different TcRVbeta isoforms. We have designed three different chimeras linking the same DRalpha with different TcRVbeta isoforms to specifically target SEB, SEC3 and TSST-1 and inhibit their pathogenesis. Here, we show by molecular modeling that the DRalpha, TcRVbeta and linker of a given chimera interact with the target superantigen in a type-specific manner. An initial model of the complex is constructed on the basis of observed inter-molecular contacts between DRalpha/TcRVbeta and the superantigens. A constant temperature (300 K) 200 ps molecular dynamics is performed to sample different conformations of a chimera-superantigen complex by utilizing the flexibility of the (GSTAPPA)(2) linker while maintaining the native folds of superantigen, DRalpha and TcRVbeta and the observed intermolecular contacts. After equilibration, 100 molecular dynamic snapshots are minimized and analyzed. This provides descriptions of various pairwise interactions at the contact interface in the complex and important clues on single site mutations on the chimera that may enhance the stability of a given superantigen-chimera complex., (Copyright 2004 John Wiley & Sons, Ltd.)

The Staphylococcus aureus enterotoxins (S.E.) A-I, and toxic-shock syndrome toxin TSST-1 act as superantigens to cause overstimulation of the host immune system, leading to the onset of various diseases including food poisoning and toxic shock syndrome. SAgs bind as intact proteins to the DRalpha1 domain of the MHC class II receptor and the TcRVbeta domain from the T cell receptor and cause excessive release of cytokines such as IL-2, TNF-alpha, and IFN-gamma, and hyperproliferation of T cells. In addition, different SAgs bind and activate different TcRVbeta isoforms during pathogenesis of human immune cells. These two properties of SAgs prompted us to design several chimeric DRalpha1-linker-TcRVbeta proteins using different TcRVbeta isoforms to create chimeras that would specifically inhibit the pathogenesis of SAgs against which they were designed. In this study, we compare the design, interaction, and inhibitory properties of three different DRalpha1-linker-TcRVbeta chimeras targeted against three different SAgs, SEB, SEC3, and TSST-1. The inhibitory properties of the chimeras were tested by monitoring IL-2 release and T cell proliferation using a primary human cell model. We demonstrate that the three chimeras specifically inhibit the pathogenesis of their target superantigen. We performed molecular modeling to analyze the structural basis of the type specificity exhibited by different chimeras designed against their target SAgs, examine the role of the linker in determining binding and specificity, and suggest site-specific mutations in the chimera to enhance binding affinity. The fact that our strategy works equally well for SEB and TSST-1, two widely different phylogenic variants, suggests that the DRalpha1-linker-TcRVbeta chimeras may be developed as a general therapy against a broad spectrum of superantigens released during Staphylococcal infection.