Active fault scarps in southern Malawi and their implications for the distribution of strain in incipient continental rifts

The distribution of deformation during the early stages of continental rifting is an important constraint on our understanding of continental breakup. Incipient rifting in East Africa has been considered to be dominated by slip along rift border faults, with a subsequent transition to focussed extension on axial segments in thinned crust and/or with active magmatism. Here, we study high‐resolution satellite data of the Zomba Graben in southern Malawi, an amagmatic rift whose topography is dominated by the west‐dipping Zomba fault. We document evidence for five sub‐parallel fault scarps between 13 and 51 km long spaced ~10‐15 km apart. The scarps consist of up to five segments between 4‐18 km long, separated by minima in scarp height and river knickpoints. The maximum height of each fault scarp ranges from 9.5 ± 4.2 m to 35.3 ± 14.6 m, with the highest scarp measured on the intrabasin Chingale Step fault. We estimate that the scarps were formed by multiple earthquakes of up to Mw7.1, and represent a previously unrecognized seismic hazard. Our calculations show that 55 ± 24 % of extensional strain is accommodated across intrabasin faults within the ~50 km wide rift. This demonstrates that a significant proportion of displacement can occur on intrabasin faults during early stage rifting, even in thick continental lithosphere with no evidence for magmatic fluids

Fault-based probabilistic seismic hazard analysis in regions with low strain rates and a thick seismogenic layer: a case study from Malawi

Historical and instrumental earthquake catalogs in low strain rate regions are not necessarily indicative of the long-term spatio-temporal distribution of seismicity. This implies that probabilistic seismic hazard analysis (PSHA) should also consider geologic and geodetic data through fault-based seismogenic sources. However, it is not always clear how on-fault magnitude-frequency distributions (MFDs) should be described and, if the seismogenic layer is especially thick, how fault sources should be extrapolated down-dip. We explore these issues in the context of a new PSHA for Malawi, where regional extensional rates are 0.5–2 mm yr−1, the seismogenic layer is 30–40-km thick, the instrumental catalog is ∼60 yr long and fault-based sources were recently collated in the Malawi Seismogenic Source Model. Furthermore, Malawi is one of several countries along the East African Rift where exposure to seismic hazard is growing, but PSHA does not typically consider fault sources. We use stochastic event catalogs to explore different fault source down-dip extents and MFDs. Our PSHA indicates that hazard levels are highest for a Gutenberg–Richter on-fault MFD, even at low probabilities of exceedance (2 per cent in 50 yr), whilst seismic hazard levels are also sensitive to how relatively short (<50 km) fault sources are extrapolated down-dip. For sites close to fault sources (<40 km), seismic hazard levels are doubled compared to previous instrumental-seismicity based PSHA in Malawi. Cumulatively, these results highlight the need for careful fault source modelling in PSHA of low strain rate regions and the need for new fault-based PSHA elsewhere in the East Africa Rift

A database of the coseismic effects following the 30 October 2016 Norcia earthquake in Central Italy

We provide a database of the coseismic geological surface effects following the Mw 6.5 Norcia earthquake that hit central Italy on 30 October 2016. This was one of the strongest seismic events to occur in Europe in the past thirty years, causing complex surface ruptures over an area of >400 km 2. The database originated from the collaboration of several European teams (Open EMERGEO Working Group; about 130 researchers) coordinated by the Istituto Nazionale di Geofisica e Vulcanologia. The observations were collected by performing detailed field surveys in the epicentral region in order to describe the geometry and kinematics of surface faulting, and subsequently of landslides and other secondary coseismic effects. The resulting database consists of homogeneous georeferenced records identifying 7323 observation points, each of which contains 18 numeric and string fields of relevant information. This database will impact future earthquake studies focused on modelling of the seismic processes in active extensional settings, updating probabilistic estimates of slip distribution, and assessing the hazard of surface faulting

Neutrophil depletion reduces edema formation and tissue loss following traumatic brain injury in mice

Background: Brain edema as a result of secondary injury following traumatic brain injury (TBI) is a major clinical concern. Neutrophils are known to cause increased vascular permeability leading to edema formation in peripheral tissue, but their role in the pathology following TBI remains unclear. Methods: In this study we used controlled cortical impact (CCI) as a model for TBI and investigated the role of neutrophils in the response to injury. The outcome of mice that were depleted of neutrophils using an anti-Gr-1 antibody was compared to that in mice with intact neutrophil count. The effect of neutrophil depletion on blood-brain barrier function was assessed by Evan's blue dye extravasation, and analysis of brain water content was used as a measurement of brain edema formation (24 and 48 hours after CCI). Lesion volume was measured 7 and 14 days after CCI. Immunohistochemistry was used to assess cell death, using a marker for cleaved caspase-3 at 24 hours after injury, and microglial/macrophage activation 7 days after CCI. Data were analyzed using Mann-Whitney test for non-parametric data. Results: Neutrophil depletion did not significantly affect Evan's blue extravasation at any time-point after CCI. However, neutrophil-depleted mice exhibited a decreased water content both at 24 and 48 hours after CCI indicating reduced edema formation. Furthermore, brain tissue loss was attenuated in neutropenic mice at 7 and 14 days after injury. Additionally, these mice had a significantly reduced number of activated microglia/macrophages 7 days after CCI, and of cleaved caspase-3 positive cells 24 h after injury. Conclusion: Our results suggest that neutrophils are involved in the edema formation, but not the extravasation of large proteins, as well as contributing to cell death and tissue loss following TBI in mice