Upper-plate conduits linked to plate boundary that hosts slow earthquakes.

In shallow subduction zones, fluid behavior impacts various geodynamic processes capable of regulating slip behaviors and forming mud volcanoes. However, evidence of structures that control the fluid transfer within an overriding plate is limited and the physical properties at the source faults of slow earthquakes are poorly understood. Here we present high-resolution seismic velocity models and reflection images of the Hyuga-nada area, Japan, where the Kyushu-Palau ridge subducts. We image distinct kilometer-wide columns in the upper plate with reduced velocities that extend vertically from the seafloor down to 10-13 km depth. We interpret the low-velocity columns as damaged zones caused by seamount subduction and suggest that they serve as conduits, facilitating vertical fluid migration from the plate boundary. The lateral variation in upper-plate velocity and seismic reflectivity along the plate boundary correlates with the distribution of slow earthquakes, indicating that the upper-plate drainage system controls the complex pattern of seismic slip at subduction faults.

Presence of interplate channel layer controls of slip during and after the 2011 Tohoku-Oki earthquake through the frictional characteristics.

There are significant differences between the middle and southern segments of the Japan Trench in terms of the seismic and aseismic slips on the plate interface and seismic velocity structures. Although the large coseismic slip of the 2011 Tohoku-Oki earthquake was limited to the middle segment, the observed negative residual gravity anomaly area in the southern segment corresponds to the postseismic slip area of the Tohoku-Oki earthquake. A density distribution model can explain the different slip behaviours of the two segments by considering their structural differences. The model indicates that the plate interface in the south was covered with a thick channel layer, as indicated by seismic survey imaging, and this layer resulted in a residual gravity anomaly. Numerical simulations which assumed evident frictional heterogeneity caused by the layer in the south efficiently reproduced M9 earthquakes recurring only in the middle, followed by evident postseismic slips in the south. This study proposes that although the layer makes the megathrust less compliant to seismic slip, it promotes aseismic slips following the growth of seismic slips on the fault in an adjacent region.

Correlation of frontal prism structures and slope failures near the trench axis with shallow megathrust slip at the Japan Trench.

Since the giant 2011 Tohoku earthquake and tsunami, much research has focused on the distribution of coseismic slip at shallow depths during this subduction megathrust event. Here we present seismic images obtained in the immediate vicinity of the trench axis, that show thrust faults and fold-and-thrust type deformation structures near the epicenter of the 2011 Tohoku earthquake where the large coseismic slip has been inferred, and chaotic structure and the absence of thrust faults in northern and southern source areas. Seismic profiles show evidence of slope failures of the trench inner wall in a proposed tsunami source region around 39°-40° N, where the slips estimated from previous studies are in disagreement. Our results show that structural characteristics in the trench axis may be related to the occurrence of shallow megathrust slip and tsunamigenesis in the Japan Trench.

Controlling factor of incoming plate hydration at the north-western Pacific margin.

Hydration of the subducting oceanic plate determines the amount of water transported from Earth's surface into its interior, and plate bending-related faulting (bend faulting) just prior to subduction is considered to promote hydration. Bend faulting shows significant spatial variation, but its contribution to hydration is still poorly understood. Here we present the results of controlled-source seismic surveys around the junction of the Japan and Kuril trenches. We found structural changes caused by bend faulting before subduction differed distinctly between both trenches and were well correlated with plate hydration after subduction, suggesting the bend faulting controls spatial variations in plate hydration. Differences in bend faulting are closely related to the angle between the current trench and the ancient spreading ridge, and the hydration is more extensive where this trench-ridge angle is oblique in the study area. Thus, we propose this angle is a major factor controlling plate hydration.

Evidence for frozen melts in the mid-lithosphere detected from active-source seismic data.

The interactions of the lithospheric plates that form the Earth's outer shell provide much of the evidentiary basis for modern plate tectonic theory. Seismic discontinuities in the lithosphere arising from mantle convection and plate motion provide constraints on the physical and chemical properties of the mantle that contribute to the processes of formation and evolution of tectonic plates. Seismological studies during the past two decades have detected seismic discontinuities within the oceanic lithosphere in addition to that at the lithosphere-asthenosphere boundary (LAB). However, the depth, distribution, and physical properties of these discontinuities are not well constrained, which makes it difficult to use seismological data to examine their origin. Here we present new active-source seismic data acquired along a 1,130 km profile across an old Pacific plate (148-128 Ma) that show oceanic mid-lithosphere discontinuities (oceanic MLDs) distributed 37-59 km below the seafloor. The presence of the oceanic MLDs suggests that frozen melts that accumulated at past LABs have been preserved as low-velocity layers within the current mature lithosphere. These observations show that long-offset, high-frequency, active-source seismic data can be used to image mid-lithospheric structure, which is fundamental to understanding the formation and evolution of tectonic plates.

Structure of the tsunamigenic plate boundary and low-frequency earthquakes in the southern Ryukyu Trench.

It has been recognized that even weakly coupled subduction zones may cause large interplate earthquakes leading to destructive tsunamis. The Ryukyu Trench is one of the best fields to study this phenomenon, since various slow earthquakes and tsunamis have occurred; yet the fault structure and seismic activity there are poorly constrained. Here we present seismological evidence from marine observation for megathrust faults and low-frequency earthquakes (LFEs). On the basis of passive observation we find LFEs occur at 15-18 km depths along the plate interface and their distribution seems to bridge the gap between the shallow tsunamigenic zone and the deep slow slip region. This suggests that the southern Ryukyu Trench is dominated by slow earthquakes at any depths and lacks a typical locked zone. The plate interface is overlaid by a low-velocity wedge and is accompanied by polarity reversals of seismic reflections, indicating fluids exist at various depths along the plate interface.

Histamine mediates the stimulatory action of ghrelin on acid secretion in rat stomach.

Ghrelin, a novel growth hormone-releasing peptide, is present in the rat and human stomach and is known to stimulate acid secretion and stomach motility. However, the mechanism of action of ghrelin is not fully understood. In the present study, we attempted to elucidate the role of histamine in ghrelin-induced acid secretion in rat stomach. Intravenous administration of ghrelin at 0.8 to 20 microg/kg dose dependently increased gastric acid secretion, as measured by the gastric lumen perfusion method. The maximum response was almost equal to that of gastrin (20 microg/kg). These actions were abolished by bilateral subdiaphragmatic vagotomy. Famotidine (0.33 mg/kg) also completely inhibited the effects of ghrelin. Furthermore, ghrelin increased histidine decarboxylase (HDC) messenger RNA (mRNA) levels, as measured by real-time reverse transcription-polymerase chain reaction using LightCycler. The action of ghrelin on HDC mRNA was abolished by vagotomy. Ghrelin did not affect histamine release from isolated vascularly perfused rat stomach. Taken together, these results suggest that ghrelin stimulates gastric acid secretion via a mechanism involving activation of vagal efferent nerve and histamine release from gastric enterochromaffin-like cells.

Effect of interleukin-8 on histamine release from totally isolated vascularly perfused rat stomach.

BACKGROUND: Recent studies have demonstrated relationships between cytokines and gastric acid secretion. The present study was performed in rats to elucidate the effects of interleukin-8 (IL-8) on gastric acid secretion through an increase in histamine release from the stomach. METHODS: The experiments were performed in gastric lumen-perfused rats for the study of acid secretion and in totally isolated vascularly perfused rat stomach preparations for the study of histamine release. The histamine in the effluent was determined by radioimmunoassay. RESULTS: IL-8 (500 ng) significantly enhanced gastrin-stimulated acid secretion. IL-8, at a concentration of 500 ng/20 ml per 10 min, did not alter basal histamine release, but at 100 ng/20 ml and 500 ng/20 ml it dose-dependently increased gastrin-stimulated histamine release. CONCLUSIONS: IL-8 enhances gastrin-stimulated acid secretion and histamine release from the rat stomach, which may explain the enhancing effect of IL-8 on gastric acid secretion.

Neutrophil-derived hydroxyl radicals mediate interleukin-8-induced increases in tetragastrin-stimulated acid secretion in rats.

Until recently, the secretion of gastric acid, which plays an important role in the pathogenesis of peptic ulcer, was thought to be controlled by diet, the autonomic nerves and gut hormones. However, peptic ulcer is now known to be caused by the infection with Helicobacter pylori (H. pylori), so it is possible that inflammation modifies the secretion of gastric acid. We used gastric-lumen-perfused rats to first examine the effect of interleukin-8 (IL-8) on acid secretion and then the involvement of free radicals and neutrophils in the action of IL-8. IL-8 enhanced tetragastrin-stimulated acid secretion and free radical scavengers or inhibitors and the pretreatment with anti-rat neutrophil serum inhibited this effect, which indicates that IL-8 enhances gastrin-stimulated acid secretion and that neutrophil-derived hydroxyl radicals mediate the IL-8-induced increase in acid secretion.