Lower plate structure and upper plate deformational segmentation at the Sunda-Banda arc transition, Indonesia

The Sunda‐Banda arc transition at the eastern termination of the Sunda margin (Indonesia) represents a unique natural laboratory to study the effects of lower plate variability on upper plate deformational segmentation. Neighboring margin segments display a high degree of structural diversity of the incoming plate (transition from an oceanic to a continental lower plate, presence/absence of an oceanic plateau, variability of subducting seafloor morphology) as well as a wide range of corresponding fore‐arc structures, including a large sedimentary basin and an accretionary prism/outer arc high of variable size and shape. Here, we present results of a combined analysis of seismic wide‐angle refraction, multichannel streamer and gravity data recorded in two trench normal corridors located offshore the islands of Lombok (116°E) and Sumba (119°E). On the incoming plate, the results reveal a 8.6–9.0 km thick oceanic crust, which is progressively faulted and altered when approaching the trench, where upper mantle velocities are reduced to ∼7.5 km/s. The outer arc high, located between the trench and the fore‐arc basin, is characterized by sedimentary‐type velocities (Vp < 5.5 km/s) down to the top of the subducting slab (∼13 km depth). The oceanic slab can be traced over 70–100 km distance beneath the fore arc. A shallow serpentinized mantle wedge at ∼16 km depth offshore Lombok is absent offshore Sumba, where our models reveal the transition to the collisional regime farther to the east and to the Sumba block in the north. Our results allow a detailed view into the complex structure of both the deeper and shallower portions of the eastern Sunda margin

Deep water recycling through time

We investigate the dehydration processes in subduction zones and their implications for the water cycle throughout Earth's history. We use a numerical tool that combines thermo-mechanical models with a thermodynamic database to examine slab dehydration for present-day and early Earth settings and its consequences for the deep water recycling. We investigate the reactions responsible for releasing water from the crust and the hydrated lithospheric mantle and how they change with subduction velocity (vs), slab age (a) and mantle temperature (Tm). Our results show that faster slabs dehydrate over a wide area: they start dehydrating shallower and they carry water deeper into the mantle. We parameterize the amount of water that can be carried deep into the mantle, W (×105 kg/m2), as a function of vs (cm/yr), a (Myrs), and Tm (°C): inline image. We generally observe that a 1) 100°C increase in the mantle temperature, or 2) ∼15 Myr decrease of plate age, or 3) decrease in subduction velocity of ∼2 cm/yr all have the same effect on the amount of water retained in the slab at depth, corresponding to a decrease of ∼2.2×105 kg/m2 of H2O. We estimate that for present-day conditions ∼26% of the global influx water, or 7×108 Tg/Myr of H2O, is recycled into the mantle. Using a realistic distribution of subduction parameters, we illustrate that deep water recycling might still be possible in early Earth conditions, although its efficiency would generally decrease. Indeed, 0.5–3.7 × 108 Tg/Myr of H2O could still be recycled in the mantle at 2.8 Ga

Transmission of Amyloidosis in Offspring of Mice with AApoAII Amyloidosis

Pre-existing amyloid fibrils can induce further polymerization of endogenous precursor proteins in vivo. Thus, transmission of amyloid fibrils (AApoAII) may induce a conformational change in endogenous apolipoprotein A-II and accelerate amyloid deposition in mouse senile amyloidosis. To characterize transmissibility, we examined amyloidosis in the offspring of AApoAII-injected mother mice that possessed the amyloidogenic Apoa2(c) allele of the apolipoprotein A-II gene. At 4 months of age, amyloid deposits were detected in the intestines of offspring born from and nursed by amyloid fibril-injected mothers, with intensity of deposition increasing thereafter. No amyloid deposits were detected in the offspring of noninjected control mothers. Accelerated amyloidosis was also observed in offspring born from mothers without injection but nursed by amyloid fibril-injected mothers. However, this was not observed in offspring born from amyloid fibril-injected mothers but nursed by control mothers. This fostering excluded vertical transmission through the placenta, suggesting the presence of factors that accelerate amyloidosis during the nursing period. In addition, milk obtained from amyloid fibril-injected mothers induced AApoAII amyloidosis in young mice, and transmission electron microscopy detected noodle-like amyloid fibrils in milk of amyloid fibril-injected mothers. These results provide important insight into the etiology and pathogenesis of amyloid diseases