Temporal stability of coda Q in the northeastern part of an inland high strain rate zone, central Japan: implication of a persistent ductile deformation in the crust

金沢大学理工研究域地球社会基盤学系We have analyzed the temporal variation in coda Q in the northeastern part of an inland high strain rate zone, the Niigata–Kobe Tectonic Zone (NKTZ), in central Japan, to investigate the response of coda Q to the modification of the strain field induced by the 2011 Tohoku earthquake (Mw 9.0). We observe no statistically significant temporal variations in the spatial distribution of coda Q as the whole analyzed area, implying that the crustal deformation induced by the 2011 Tohoku earthquake has provided no significant temporal variation in crustal heterogeneity as the whole analyzed area. For the middle frequency bands, before and after the 2011 Tohoku earthquake, we have commonly found a negative correlation between the spatial distributions of coda Q and the differential strain rate and a positive correlation between the spatial distributions of coda Q and the perturbation of S-wave velocity in the upper crust. These features, together with previous works, suggest that the ductile deformation with a high rate in the upper crust plays an important role in generating the high strain rate in the analyzed area not only before but also after the 2011 Tohoku earthquake. In other words, the existence of a persistent ductile deformation in the upper crust contributes essentially to the generation process of the high strain rate in the northeastern part of the NKTZ. It is important to note that the location of the persistent ductile deformation in the northeastern part of the NKTZ, mainly in the upper crust, differs from that in the central part of the NKTZ, mainly in the lower crust.Japan Society for the Promotion of Science 26109000

Inhibitory Effects of Lidocaine and Mexiletine on Vasorelaxation Mediated by Adenosine Triphosphate-sensitive K ؉ Channels and the Role of Kinases in the Porcine Coronary Artery

Background: Effects of antiarrhythmic drugs on coronary vasodilation mediated by K ؉ channels have not been studied

Hyaluronan Export through Plasma Membranes Depends on Concurrent K+ Efflux by Kir Channels

Hyaluronan is synthesized within the cytoplasm and exported into the extracellular matrix through the cell membrane of fibroblasts by the MRP5 transporter. In order to meet the law of electroneutrality, a cation is required to neutralize the emerging negative hyaluronan charges. As we previously observed an inhibiting of hyaluronan export by inhibitors of K+ channels, hyaluronan export was now analysed by simultaneously measuring membrane potential in the presence of drugs. This was done by both hyaluronan import into inside-out vesicles and by inhibition with antisense siRNA. Hyaluronan export from fibroblast was particularly inhibited by glibenclamide, ropivacain and BaCl2 which all belong to ATP-sensitive inwardly-rectifying Kir channel inhibitors. Import of hyaluronan into vesicles was activated by 150 mM KCl and this activation was abolished by ATP. siRNA for the K+ channels Kir3.4 and Kir6.2 inhibited hyaluronan export. Collectively, these results indicated that hyaluronan export depends on concurrent K+ efflux

Spatial variation in coda Q in the northeastern part of Niigata–Kobe Tectonic Zone, central Japan: implication of the cause of a high strain rate zone

Abstract We have analyzed the spatial variation in coda Q in the northeastern part of a high strain rate zone, the Niigata–Kobe Tectonic Zone (NKTZ), to investigate the cause of the high strain rate by correlating coda Q with the differential strain rate and the S-wave velocity. The spatial distributions of coda Q in the 2–4 and 4–8 Hz frequency bands are found to be negatively correlated with the differential strain rate. Coda Q in the 2–4 Hz frequency band is correlated spatially with the S-wave velocity at a 25 km depth, as has been reported previously. We also find a positive correlation between the perturbation of the S-wave velocity at a 10 km depth and coda Q in the 4–8 Hz frequency band, implying that the spatial distribution of coda Q in this frequency band is mainly attributed to the heterogeneity of the upper crust. This feature is different from that of the central part of the NKTZ reported previously, which indicates a difference in the cause of the high strain rate. Therefore, we suggest that the high deformation rate in the upper crust, which is characterized by a thick sediment basin, as well as that in the ductile lower crust, contributes to the generation process of the high strain rate on the surface in the northeastern part of the NKTZ. Graphical abstract

Temporal stability of coda Q in the northeastern part of an inland high strain rate zone, central Japan: implication of a persistent ductile deformation in the crust

Abstract We have analyzed the temporal variation in coda Q in the northeastern part of an inland high strain rate zone, the Niigata–Kobe Tectonic Zone (NKTZ), in central Japan, to investigate the response of coda Q to the modification of the strain field induced by the 2011 Tohoku earthquake (Mw 9.0). We observe no statistically significant temporal variations in the spatial distribution of coda Q as the whole analyzed area, implying that the crustal deformation induced by the 2011 Tohoku earthquake has provided no significant temporal variation in crustal heterogeneity as the whole analyzed area. For the middle frequency bands, before and after the 2011 Tohoku earthquake, we have commonly found a negative correlation between the spatial distributions of coda Q and the differential strain rate and a positive correlation between the spatial distributions of coda Q and the perturbation of S-wave velocity in the upper crust. These features, together with previous works, suggest that the ductile deformation with a high rate in the upper crust plays an important role in generating the high strain rate in the analyzed area not only before but also after the 2011 Tohoku earthquake. In other words, the existence of a persistent ductile deformation in the upper crust contributes essentially to the generation process of the high strain rate in the northeastern part of the NKTZ. It is important to note that the location of the persistent ductile deformation in the northeastern part of the NKTZ, mainly in the upper crust, differs from that in the central part of the NKTZ, mainly in the lower crust

Regulation of necroptotic-apoptotic signaling in vitro and in vivo

Programmed cell death (PCD) is an evolutionarily conserved process observable in all metazoans. In mammals this process is requisite for organ and structural development of the fetus, pathogen clearance, tissue remodeling and homeostasis, responses to cellular stress, and suppression of oncogenesis. Several major forms of PCD have been characterized to date, including apoptosis, necroptosis and autophagy-dependent cell death (ADCD). Each of these forms of PCD demonstrate their own morphologic and molecular features. In particular, apoptotic and necroptotic cell death have been identified in many circumstances to be competitive in nature, often displaying a ‘winner take all’ dynamic where necroptosis provides a backup role in many tissues upon failure of apoptosis. To better understand the regulation of PCD and more specifically the interactions between apoptosis and necroptosis, I have examined these forms of cell death in two models: (1) cisplatin-mediated cell death of homogeneous populations of embryonic stem (ES) cells in vitro and (2) endothelin-1 mediated ischemic/reperfusion injury in the murine cortex in vivo. In addition to homologous gene recombination, I have also utilized pharmacologic inhibitors to interrogate the interaction of these pathways in detail for both models. Using these methods, I demonstrate that ES cells exposed to cisplatin demonstrate a hitherto uncharacterized novel form of cooperative PCD between apoptotic caspase-3 and necroptotic RIPK1 and RIPK3. Further analyses suggest that RIPK1 and RIPK3 signaling lie upstream of caspase-3 in this cooperative pathway and that the resulting cell morphology and molecular details of dead/dying cells reflect neither traditional apoptosis nor necroptosis, instead demonstrating a hybrid of both. Characterization of the neuronal cell death involved in endothelin-1-mediated cortical ischemic/reperfusion injury in vivo was similarly observed to be protected through inhibition of either RIPK1 or caspase-3. Interestingly, protection induced by inhibition of RIPK1 seem to occur upstream of caspase-3-mediated apoptosis similar to features observed in ES cells. This identification of a novel co-operative apoptotic/necroptotic signaling in turn have important implications for cell death regulation in primary tissues – in terms of both pathologic processes and pharmacologic interventions.Ph.D.2021-11-30 00:00:0