Fluidised landslides are one of the most dangerous types of mass movements as they can run over long distances at high velocity. A flow-like landslide can occur in both artificially designed and natural slopes, resulting in extensive property damage and significant loss of life. Although various studies have examined the initiation mechanism of this type of landslide, the understanding of the phenomenon of instability which can occur in loose granular slopes deserves further attention. Specific influential factors, such as the changes in the soil microstructure due to water infiltration and seepage forces, still need to be further examined. In this study, the initiation of a fluidised landslide is investigated through flume tests. The tested material was collected from a coseismic landslide deposit in the 2008 Wenchuan earthquake area. These loose, granular deposits can fail due to intense rainfall and exhibit flow-like movement, potentially evolving into destructive debris flows. Two flume apparatuses have been used, which were equipped with multiple sensors to evaluate the pore pressures and the internal displacements. A high-sensitivity seismic accelerometer was installed at the bottom of the flume to record the vibrations produced by the movement of the soil particles during the tests. The soil mass was progressively wetted either by a uniform inflow from the ground surface at the top of the slope, to simulate the infiltration of run-off water arriving from upslope, or by a gradual rise of the water level at the upper boundary of the slope, to simulate a gradual rise of the groundwater table. Internal erosion of the finer soil fraction driven by the seepage forces is thought to have played a significant role in the slope collapse. Possible changes in the particle arrangement were recorded by the accelerometers in the form of an increasing high-frequency vibration signal before any significant rise of pore pressure and any significant displacement of the slope could be observed. Although further parametric investigation is still necessary, and tests at real scale should be devised, the observed behaviour suggests that seismic monitoring of loose, granular deposits could be a promising method for detecting an incipient slope collapse.
BackgroundReperfusion ventricular arrhythmia (RA) associated with hypothermic ischaemic storage is increasingly recognized as a substantial contributor to adverse consequences after heart transplantation. Ischemia- or hypothermia-induced gap junction (GJ) remodelling is closely linked to RA. Reducing GJ remodelling contributes to RA attenuation and is important in heart transplantation. However, sevoflurane has an antiarrhythmic effect associated with the connexin 43 (Cx43) protein that has not yet been fully established.MethodsHearts were divided into two groups according to a random number table: all hearts were arrested by an infusion of histidine-tryptophan-ketoglutarate (HTK) solution (4 °C) followed by (1) storage in HTK solution (4 °C) alone for 6 h (n = 8, Control group) or (2) storage in HTK solution supplemented with sevoflurane (2.5%) (4 °C) for 6 h (n = 8, Sevo-HTK group). First, the total Cx43 level and the phosphorylation of Cx43 at Ser368 (Cx43-pS368) were assessed by Western blotting, and the distribution of Cx43 was assessed by immunohistochemistry. Second, programmed electrical stimulation (PES) and monophasic action potential (MAP) recording were used to analyse the MAP duration (MAPD), conduction velocity (CV) and transmural repolarization dispersion (TDR). In addition, haematoxylin and eosin (HE) and terminal deoxynucleotidyl transferase-dUTP nick end labelling (TUNEL) staining were individually used to investigate the degree of myocardial pathological damage and cell apoptosis. Finally, bipolar electrograms were used to record the graft re-beating time and monitor RA during reperfusion for 15 to 30 min.ResultsSevo-HTK solution relatively increased the total Cx43 (P < 0.01) and Cx43-pS368 (P < 0.01) levels and prevented Cx43 redistribution (P < 0.05) and CV slowing (P < 0.001) but did not change TDR (P > 0.05). Additionally, the Cx43-pS368/total Cx43 ratio (P>0.05) was similar in the two groups. However, with Sevo-HTK solution, the graft re-beating times were shortened, myocardial pathological damage was ameliorated, and the number of apoptotic cells was markedly decreased.ConclusionThe reduction in hypothermia and ischaemia-induced reperfusion arrhythmias by the addition of sevoflurane to HTK solution may be related to the phosphorylation of Cx43 at serine 368.
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