Earthquakes trigger the eruption of mud and magmatic volcanoes and influence ongoing eruptive activity. One mechanism that could trigger an eruption is clay liquefaction. Here we model the propagation of seismic waves beneath the Lusi mud eruption (East Java, Indonesia) using available seismic velocity and density models to assess the effect of subsurface structure on the amplification of incident seismic waves. We find that using an updated subsurface density and velocity structure, there is no significant amplification of incident seismic energy in the Upper Kalibeng Formation, the source of the erupting solids. Hence, the hypothesis that the Lusi eruption was triggered by clay liquefaction appears unlikely to be correct. Independent constraints from gas chemistry as well as analyses of drilling activities at the nearby Banjar-Panji 1 gas exploration well and an analysis of the effects of other earthquakes all favor a drilling trigger.

The cause of the Lusi mud eruption remains controversial. The review by Miller and Mazzini (2017) firmly dismisses a role of drilling operations at the adjacent Banjarpanji-1 well and argues that the eruption was triggered by the M6.3 Yogyakarta earthquake some 254 km away. We disagree with these conclusions. We review drilling data and the daily drilling reports, which clearly confirm that the wellbore was not intact and that there was a subsurface blowout. Downhole pressure data from Lusi directly witness the birth of Lusi at the surface on the 29th of May 2006, indicating a direct connection between the well and the eruption. Furthermore, the daily drilling reports specifically state that Lusi activity was visibly altered on three separate occasions by attempts to kill the eruption by pumping dense fluid down the BJP-1 well, providing further evidence of a connection between the wellbore and Lusi. By comparison with other examples of newly initiated mud eruptions elsewhere by other earthquakes, the Yogyakarta earthquake was far away given its magnitude. The seismic energy density of the Yogyakarta earthquake was only 0.0043 J/m3, which is less than a quarter of the minimum 0.019 J/m3 seismic energy density that has ever been inferred to trigger other mud eruptions. We show that the Lusi area had previously experienced other shallow earthquakes with similar frequencies and stronger ground shaking that did not trigger an eruption. Finally, the data from the BJP-1 well indicates that there was no prior hydrodynamic connection between deep overpressured hydrothermal fluids and the shallow Kalibeng clays, and that there was no evidence of any liquefaction or remobilization of the Kalibeng clays induced by the earthquake. We thus strongly favor initiation by drilling and not an earthquake.

We present in this study a first analysis of the astrometric error budget of absolute astrometry relative to back- ground galaxies using adaptive optics. We use for this analysis multi-conjugated adaptive optics (MCAO) images obtained with GeMS/GSAOI at Gemini South. We find that it is possible to obtain 0.3 mas reference precision in a random field with 1 hour on source using faint background galaxies. Systematic errors are correctable below that level, such that the overall error is approximately 0.4 mas. Because the reference sources are extended, we find it necessary to correct for the dependency of the PSF centroid on the used aperture size, which would oth- erwise cause an important bias. This effect needs also to be considered for Extremely Large Telescopes (ELTs). When this effect is corrected, ELTs have the potential to measure proper motions of dwarfs galaxies around M31 with 10 km/s accuracy over a baseline of 5 years.

The ODYSSEY OUTCOMES trial, comprising over 47 000 patient-years of placebo-controlled observation, demonstrated important reductions in the risk of recurrent ischaemic cardiovascular events with the monoclonal antibody to proprotein convertase subtilisin/kexin type 9 alirocumab, as well as lower all-cause death. These benefits were observed in the context of substantial and persistent lowering of low-density lipoprotein cholesterol with alirocumab compared with that achieved with placebo. The safety profile of alirocumab was indistinguishable from matching placebo except for a ∼1.7% absolute increase in local injection site reactions. Further, the safety of alirocumab compared with placebo was evident in vulnerable groups identified before randomization, such as the elderly and those with diabetes mellitus, previous ischaemic stroke, or chronic kidney disease. The frequency of adverse events and laboratory-based abnormalities was generally similar to that in placebo-treated patients. Thus, alirocumab appears to be a safe and effective lipid-modifying treatment over a duration of at least 5 years.