Rapid localized flank inflation and implications for potential slope instability at Tungurahua volcano, Ecuador

This is the final version. Available on open access from Elsevier via the DOI in this recordHigh rates of volcano surface deformation can be indicative of a forthcoming eruption, but can also relate to slope instability and possible flank collapse. Tungurahua volcano, Ecuador, has been persistently active since 1999 and has previously experienced catastrophic flank failures. During the ongoing eruptive activity, significant surface deformation has been observed, with the highest rates contained within the amphitheatre-shaped scar from the 3000-year-old failure on the west flank However, the cause of this asymmetric deformation and how it might relate to slope stability has not been assessed. Here, for the first time, we present a range of models to test physical processes that might produce asymmetric deformation, which are then applied to slope stability. Our models are informed by InSAR measurements of a deformation episode in November 2015, which show a maximum displacement of ~3.5 cm over a period of ~3 weeks, during which time the volcano also experienced multiple explosions and heightened seismicity. Asymmetric flank material properties, from the rebuilding of the cone, cannot explain the full magnitude and spatial footprint of the observed west flank deformation. The inflation is inferred to be primarily caused by shallow, short35 term, pre-eruptive magma storage that preferentially exploits the 3 ka flank collapse surface. Shallow and rapid pressurization from this inclined deformation source can generate shear stress along the collapse surface, which increases with greater volumes of magma. This may contribute to slope instability during future unrest episodes and promote flank failure, with general application to other volcanoes worldwide displaying asymmetric deformation patterns.Royal SocietyNatural Environment Research Council (NERC)Economic and Social Research Council (ESRC

Protect or perish: Quantitative analysis of state-level species protection supports preservation of the Endangered Species Act

To combat biodiversity loss in the United States, imperiled species are protected under the federal Endangered Species Act (ESA), which is currently threatened by political initiatives seeking to weaken it and potentially transfer substantial authority to the states. To assess the conservation capacity of current state laws, we conducted a quantitative analysis of imperiled species protection within all 50 states by compiling data on all state-listed species, ESA-listed species, and IUCN Red List species in each state. We found that currently 16% of ESA-listed species and 52% of IUCN imperiled species are not protected by any state law, and if the ESA were repealed these numbers could increase to 73% of ESA-listed species and 81% of IUCN imperiled species unprotected. Although protection varies widely among states, our results suggest that revoking the ESA would be highly detrimental to imperiled species conservation and recovery in the United States

A quantitative modular modeling approach reveals the effects of different A20 feedback implementations for the NF-κB signaling dynamics

Signaling pathways involve complex molecular interactions and are controled by non-linear regulatory mechanisms. If details of regulatory mechanisms are not fully elucidated, they can be implemented by different, equally reasonable mathematical representations in computational models. The study presented here focusses on NF-κB signaling, which is regulated by negative feedbacks via IκBα and A20. A20 inhibits NF-κB activation indirectly through interference with proteins that transduce the signal from the TNF receptor complex to activate the IκB kinase (IKK) complex. A number of pathway models has been developed implementing the A20 effect in different ways. We here focus on the question how different A20 feedback implementations impact the dynamics of NF-κB. To this end, we develop a modular modeling approach that allows combining previously published A20 modules with a common pathway core module. The resulting models are fitted to a published comprehensive experimental data set and therefore show quantitatively comparable NF-κB dynamics. Based on defined measures for the initial and long-term behavior we analyze the effects of a wide range of changes in the A20 feedback strength, the IκBα feedback strength and the TNFα stimulation strength on NF-κB dynamics. This shows similarities between the models but also model-specific differences. In particular, the A20 feedback strength and the TNFα stimulation strength affect initial and long-term NF-κB concentrations differently in the analyzed models. We validated our model predictions experimentally by varying TNFα concentrations applied to HeLa cells. These time course data indicate that only one of the A20 feedback models appropriately describes the impact of A20 on the NF-κB dynamics in this cell type

Antibiofilm activity of Cobetia marina filtrate upon Staphylococcus epidermidis catheter-related isolates

We report the antibiofilm activity by the sponge-associated bacterium Cobetia marina upon Staphylococcus epidermidis clinical isolates obtained from central venous catheters. Antibiofilm activity/antimicrobial susceptibility correlation might predict the action of the metabolite(s) upon Staphylococcus epidermidis in the clinic, making it a possible adjuvant in therapies against biofilm-associated infections

RC3H1 post-transcriptionally regulates A20 mRNA and modulates the activity of the IKK/NF-kappa B pathway

The RNA-binding protein RC3H1 (also known as ROQUIN) promotes TNF alpha mRNA decay via a 3'UTR constitutive decay element (CDE). Here we applied PAR-CLIP to human RC3H1 to identify similar to 3, 800 mRNA targets with 416, 000 binding sites. A large number of sites are distinct from the consensus CDE and revealed a structure-sequence motif with U-rich sequences embedded in hairpins. RC3H1 binds preferentially short-lived and DNA damage-induced mRNAs, indicating a role of this RNA-binding protein in the post-transcriptional regulation of the DNA damage response. Intriguingly, RC3H1 affects expression of the NF-kappa B pathway regulators such as I kappa B alpha and A20. RC3H1 uses ROQ and Zn-finger domains to contact a binding site in the A20 30UTR, demonstrating a not yet recognized mode of RC3H1 binding. Knockdown of RC3H1 resulted in increased A20 protein expression, thereby interfering with I kappa B kinase and NF-kappa B activities, demonstrating that RC3H1 can modulate the activity of the IKK/NF-kappa B pathway