Seismic exploration at Fuji volcano with active sources : The outline of the experiment and the arrival time data

Fuji volcano (altitude 3,776m) is the largest basaltic stratovolcano in Japan. In late August and early September 2003, seismic exploration was conducted around Fuji volcano by the detonation of 500 kg charges of dynamite to investigate the seismic structure of that area. Seismographs with an eigenfrequency of 2 Hz were used for observation, positioned along a WSW-ENE line passing through the summit of the mountain. A total of 469 seismic stations were installed at intervals of 250-500 m. The data were stored in memory on-site using data loggers. The sampling interval was 4 ms. Charges were detonated at 5 points, one at each end of the observation line and 3 along its length. The first arrival times and the later-phase arrival times at each station for each detonation were recorded as data. P-wave velocities in the surface layer were estimated from the travel time curves near the explosion points, with results of 2.5 km/s obtained for the vicinity of Fuji volcano and 4.0 km5/s elsewhere

Preparatory process preceding the 2014 eruption of Mount Ontake volcano, Japan: Insights from precise leveling measurements 5.Volcanology

Preparatory activity preceding the 2014 eruption of Mount Ontake volcano was estimated from vertical deformation detected using a precise leveling survey. Notable uplift (2006-2009) and subsidence (2009-2014) were detected on the eastern flank of the volcano. We estimated pressure source models based on the vertical deformation and used these to infer preparatory process preceding the 2014 eruption. Our results suggest that the subsidence experienced between 2009 and 2014 (including the period of the 2014 eruption) occurred as a result of a sill-like tensile crack with a depth of 2.5 km. This tensile crack might inflate prior to the eruption and deflate during the 2014 activity. A two-tensile-crack model was used to explain uplift from 2006 to 2009. The geometry of the shallow crack was assumed to be the same as the sill-like tensile crack. The deep crack was estimated to be 2 km in length, 4.5 km in width, and 3 km in depth. Distinct uplifts began on the volcano flanks in 2006 and were followed by seismic activities and a small phreatic eruption in 2007. From the partially surveyed leveling data in August 2013, uplift might continue until August 2013 without seismic activity in the summit area. Based on the uplift from 2006 to 2013, magma ascended rapidly beneath the summit area in December 2006, and deep and shallow tensile cracks were expanded between 2006 and 2013. The presence of expanded cracks between 2007 and 2013 has not been inferred by previous studies. A phreatic eruption occurred on 27 September 2014, and, following this activity, the shallow crack may have deflated

S1P3-mediated cardiac fibrosis in sphingosine kinase 1 transgenic mice involves reactive oxygen species

金沢大学医薬保健研究域医学系Aims Sphingosine kinase 1 (SPHK1), its product sphingosine-1-phosphate (S1P), and S1P receptor subtypes have been suggested to play protective roles for cardiomyocytes in animal models of ischaemic preconditioning and cardiac ischaemia/reperfusion injury. To get more insight into roles for SPHK1 in vivo, we have generated SPHK1-transgenic (TG) mice and analysed the cardiac phenotype.Methods and results SPHK1-TG mice overexpressed SPHK1 in diverse tissues, with a nearly 20-fold increase in enzymatic activity. The TG mice grew normally with normal blood chemistry, cell counts, heart rate, and blood pressure. Unexpectedly, TG mice with high but not low expression levels of SPHK1 developed progressive myocardial degeneration and fibrosis, with upregulation of embryonic genes, elevated RhoA and Rac1 activity, stimulation of Smad3 phosphorylation, and increased levels of oxidative stress markers. Treatment of juvenile TG mice with pitavastatin, an established inhibitor of the Rho family G proteins, or deletion of S1P3, a major myocardial S1P receptor subtype that couples to Rho GTPases and transactivates Smad signalling, both inhibited cardiac fibrosis with concomitant inhibition of SPHK1-dependent Smad-3 phosphorylation. In addition, the anti-oxidant N-2-mercaptopropyonylglycine, which reduces reactive oxygen species (ROS), also inhibited cardiac fibrosis. In in vivo ischaemia/reperfusion injury, the size of myocardial infarct was 30 decreased in SPHK1-TG mice compared with wild-type mice.Conclusion These results suggest that chronic activation of SPHK1-S1P signalling results in both pathological cardiac remodelling through ROS mediated by S1P3 and favourable cardioprotective effects