The discovery of slow earthquakes has revolutionized the field of earthquake seismology. Defining the locations of these events and the conditions that favor their occurrence provides important insights into the slip behavior of tectonic faults. We report on a family of recurring slow-slip events (SSEs) on the plate interface immediately seaward of repeated historical moment magnitude () 8 earthquake rupture areas offshore of Japan. The SSEs continue for days to several weeks, include both spontaneous and triggered slip, recur every 8 to 15 months, and are accompanied by swarms of low-frequency tremors. We can explain the SSEs with 1 to 4 centimeters of slip along the megathrust, centered 25 to 35 kilometers (km) from the trench (4 to 10 km depth). The SSEs accommodate 30 to 55% of the plate motion, indicating frequent release of accumulated strain near the trench.
An Mw 6.0 earthquake struck ~50 km offshore the Kii Peninsula of southwest Honshu, Japan on 1 April 2016. This earthquake occurred directly beneath a cabled offshore monitoring network at the Nankai Trough subduction zone and within 25–35 km of two borehole observatories installed as part of the International Ocean Discovery Program's NanTroSEIZE project. The earthquake's location close to the seafloor and subseafloor network offers a unique opportunity to evaluate dense seafloor geodetic and seismological data in the near field of a moderate‐sized offshore earthquake. We use the offshore seismic network to locate the main shock and aftershocks, seafloor pressure sensors, and borehole observatory data to determine the detailed distribution of seafloor and subseafloor deformation, and seafloor pressure observations to model the resulting tsunami. Contractional strain estimated from formation pore pressure records in the borehole observatories (equivalent to 0.37 to 0.15 μstrain) provides a key to narrowing the possible range of fault plane solutions. Together, these data show that the rupture occurred on a landward dipping thrust fault at 9–10 km below the seafloor, most likely on the plate interface. Pore pressure changes recorded in one of the observatories also provide evidence for significant afterslip for at least a few days following the main shock. The earthquake and its aftershocks are located within the coseismic slip region of the 1944 Tonankai earthquake (Mw ~8.0), and immediately downdip of swarms of very low frequency earthquakes in this region, illustrating the complex distribution of megathrust slip behavior at a dominantly locked seismogenic zone.
The 9,11-azo-prostanoid III [(5Z, 9a, Ila, 13E, has been obtained by synthesis and tested for biological activity in systems which are responsive to the prostaglandin endoperoxides PGH2 (I) and PGG2 (II). The azo analog III is a powerful mimic of these endoperoxides with reference to platelet aggregation and release of serotonin when added to human platelet-rich plasma. The analog III is substantially more active (about 7 fold) than PGG2 in stimulating muscle contraction in the isolated rabbit aorta strip. The very great stability of III relative to PGH2 and PGG2 and its potency as a mimic of these important substances suggest that this azo analog will be of considerable value in future studies of the prostaglandin endoperoxides. The two prostaglandin (PG) endoperoxides, PGH2 (I, Fig. 1) and PGG2 (II), derived in vio from arachidonic acid, are very potent in inducing rapid and irreversible aggregation of human platelets through release of ADP and serotonin (1-8). The endoperoxides are rapidly metabolized to a hemiacetal derivative 8-(1-hydroxy-3-oxopropyl)-9, 12L-dihydroxy-5,10-heptadecadienoic acid (PHD) in platelets, and this metabolite is released in large amounts during aggregation induced by various agents (4, 5). A physiological role of the endoperoxide system in human platelets has been established through studies demonstrating that a hemostatic defect involving an abnormal platelet release mechanism was due to deficiency of the cyclo-oxygenase responsible for endoperoxide synthesis (3). The endoperoxides are also potent stimulants of vascular (rabbit aorta and umbilical artery) and air-way smooth muscle (6).The endoperoxides PGH2 and PGG2 are intrinsically highly unstable substances (half-life, t1/2, about 5 min in aqueous solution at 370 and pH 7.4). Further, they are transformed with great rapidity enzymically [e.g., t1/2 about 10 sec in platelet-rich plasma (PRP)]. Because of the extraordinary lability of these endoperoxides and the consequent difficulties and limitations in experimental use, the design and synthesis of a stable and active analog was deemed important. The most interesting analog for initial study appeared to be the azo compound represented by formula III in Fig. 1. It was anticipated that this substance would possess very nearly the same molecular geometry as PGH2 (I), but would be indefinitely stable at pH 7 and 370. Although there was no assurance a priori that III would behave as a close mimic of PGH2 (or PGG2) rather than as an antagonist, the experimental resolution of this question itself seemed worthwhile as a step toward a better understanding of the biochemical mode of action of PGH2.MATERIALS AND METHODS The preparation of the endoperoxides PGG2 and PGH2 has been described previously (2). Blood from healthy donors, who had not taken any drugs for at least 1 week, was collected from the antecubital vein with 0.13 volume of 0.1 M trisodium citrate. After centrifugation at 200 X g for 15 min at room temperature, PRP was removed. Calcium chloride (10 ,ul 0.25 M solutio...
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