Heterogeneous stresses and deformation mechanisms at shallow crustal conditions, Hungaroa Fault Zone, Hikurangi Subduction Margin, New Zealand

The Hungaroa Fault Zone (HFZ), an inactive thrust fault along the Hikurangi Subduction Margin, accommodated large displacements (~4-10 km) at the onset of subduction in the early Miocene. Within a 40 m-wide high-strain fault core, calcareous mudstones and marls display evidence for mixed-mode viscous flow and brittle fracture, including: discrete faults; extensional veins containing stretched calcite fibers; shear veins with calcite slickenfibers; calcite foliation-boudinage structures; calcite pressure fringes; dark dissolution seams; stylolites; embayed calcite grains; and an anastomosing phyllosilicate foliation.Multiple observations indicate a heterogeneous stress state within the fault core. Detailed optical and electron backscatter diffraction-based texture analysis of syntectonic calcite veins and isoclinally folded limestone layers within the fault core reveal that calcite grains have experienced intracrystalline plasticity and interface mobility, and local subgrain development and dynamic recrystallisation. The recrystallized grain size in two calcite veins of 6.0±3.9 µm (n=1339; 1SD; HFZ-H4-5.2m_A;) and 7.2±4.2µm (n=406; 1SD; HFZ-H4-19.9m) indicate high differential stresses (~76-134 MPa). Hydrothermal friction experiments on a foliated, calcareous mudstone yield a friction coefficient of μ≍0.35. Using this friction coefficient in the Mohr-Coulomb failure criterion yields a maximum differential stress of 55 MPa at 4 km depth, assuming a minimum principal stress equal to the vertical stress, an average sediment density of 2350 kg/m3, and hydrostatic pore fluid pressure. Interestingly, calcareous microfossils within the foliated mudstone matrix are undeformed. Moreover, calcite veins are oriented both parallel to and highly oblique to the foliation, indicating spatial and/or temporal variations in the maximum principle stress azimuth.To further constrain HFZ deformation conditions, clumped isotope geothermometry was performed on six syntectonic calcite veins, yielding formation temperatures of 79.3±19.9°C (95% confidence interval). These temperatures are well below those at which dynamic recrystallisation of calcite is anticipated and exclude shear heating and the migration of hotter fluids as an explanation for dynamic recrystallisation of calcite at shallow crustal levels

Observational and theoretical evidence for frictional-viscous flow at shallow crustal levels

Along the Hikurangi Subduction Margin, accretionary prism uplift has exposed the Hungaroa fault zone, an inactive thrust developed within the Middle to Late Eocene Wanstead Formation. Within the ~33 m-wide fault core, deformation of the smectitic, calcareous mudstone matrix produced a penetrative foliation that locally wraps around clasts. Deformation occurred at temperatures constrained by syntectonic calcite vein clumped isotope thermometry, which yielded a narrow range of Δ47 values between 0.445 ± 0.024‰ and 0.482 ± 0.013‰, corresponding to a mean calcite precipitation temperature of 82−12+13 °C. Optical and scanning electron microscopy analyses reveal that calcite underwent: dissolution along stylolites and clast, vein, and microlithon margins; precipitation in foliation-parallel and foliation-perpendicular extension veins; and precipitation in hybrid veins and strain fringes. Maximum differential stress estimates obtained from calcite twin densities (44.1 ± 13.9 to 96.6 ± 20.8 MPa) are consistent with those sustainable by a cohesionless fault at ~3 km depth with a friction coefficient in the range measured for two calcareous mudstones (μ = 0.38 to 0.50) and a micrite clast (μ = 0.61 and 0.64). Marlstone clasts within the foliated calcareous mudstone matrix contain mutually cross-cutting shear fractures and extension veins with crack-seal textures, providing evidence for temporal fluctuations in shear strength resulting from pore fluid overpressure transients. At strain rates imposed during laboratory experiments, frictional sliding involves granular flow processes. Yet, calcite microstructures indicate that diffusive mass transfer played an important role in accommodating deformation. We model the fault zone rheology assuming diffusion-controlled frictional-viscous flow, with deformation at strain rates γ˙≤ 10−9 s−1 able to have taken place at very low shear stresses (τ < 10 MPa) given sufficiently short diffusion distances (d < 0.1 mm), even in the absence of pore fluid overpressures. However, if grain-scale and fracture-scale processes change the diffusion distance, fault zones deforming via frictional-viscous flow can exhibit temporally variable strain rates. Thus, our results suggest that the shallow (up-dip) limit of the seismogenic zone is not a simple function of temperature in fault zones governed by a frictional-viscous flow rheology

Drill core from seismically active sandstone gas reservoir yields clues to internal deformation mechanisms

Europe’s largest gas field, the Groningen field (the Netherlands), is widely known for induced subsidence and seismicity caused by gas pressure depletion and associated compaction of the sandstone reservoir. Whether compaction is elastic or partly inelastic, as implied by recent experiments, is a key factor in forecasting system behavior and seismic hazard. We sought evidence for inelastic deformation through comparative microstructural analysis of unique drill core recovered from the seismogenic center of the field in 2015, 50 yr after gas production started, versus core recovered before production (1965). Quartz grain fracturing, crack healing, and stress-induced Dauphiné twinning are equally developed in the 2015 and 1965 cores, with the only measurable effect of gas production being enhanced microcracking of sparse K-feldspar grains in the 2015 core. Interpreting these grains as strain markers, we suggest that reservoir compaction involves elastic strain plus inelastic compression of weak clay films within grain contacts

Human amniotic membrane as newly identified source of amniotic fluid pulmonary surfactant

Pulmonary surfactant (PS) reduces surface tension at the air-liquid interface in the alveolar epithelium of the lung, which is required for breathing and for the pulmonary maturity of the developing foetus. However, the origin of PS had never been thoroughly investigated, although it was assumed to be secreted from the foetal developing lung. Human amniotic membrane (hAM), particularly its epithelial cell layer, composes the amniotic sac enclosing the amniotic fluid. In this study, we therefore aimed to investigate a potential contribution of the cellular components of the hAM to pulmonary surfactant found in amniotic fluid. We identified that cells within the native membrane contain lamellar bodies and express all four surfactant proteins as well as ABCA3. Lipidomic profiling by nanoESI – MS/MS revealed the presence of the essential lipid species as found in PS. Also, the biophysical activity of conditioned cell culture supernatant obtained from hAM was tested with captive bubble surfactometry. hAM supernatant showed the ability to reduce surface tension, similar to human PS obtained from bronchoalveolar lavage. This means that hAM produces the essential PS-associated components and can therefore contribute as second potential source of PS in amniotic fluid aside from the foetal lung.© The Author(s) 201

Mobile phone specific electromagnetic fields induce transient DNA damage and nucleotide excision repair in serum-deprived human glioblastoma cells

Some epidemiological studies indicate that the use of mobile phones causes cancer in humans (in particular glioblastomas). It is known that DNA damage plays a key role in malignant transformation; therefore, we investigated the impact of the UMTS signal which is widely used in mobile telecommunications, on DNA stability in ten different human cell lines (six brain derived cell lines, lymphocytes, fibroblasts, liver and buccal tissue derived cells) under conditions relevant for users (SAR 0.25 to 1.00 W/kg). We found no evidence for induction of damage in single cell gel electrophoresis assays when the cells were cultivated with serum. However, clear positive effects were seen in a p53 proficient glioblastoma line (U87) when the cells were grown under serum free conditions, while no effects were found in p53 deficient glioblastoma cells (U251). Further experiments showed that the damage disappears rapidly in U87 and that exposure induced nucleotide excision repair (NER) and does not cause double strand breaks (DSBs). The observation of NER induction is supported by results of a proteome analysis indicating that several proteins involved in NER are up-regulated after exposure to UMTS; additionally, we found limited evidence for the activation of the γ-interferon pathway. The present findings show that the signal causes transient genetic instability in glioma derived cells and activates cellular defense systems.© 2018 Al-Serori et a