Preliminary geometry and kinematics of multiple surface ruptures during the 2016 MW 7.8 Kaikōura earthquake, North Canterbury region, New Zealand

The Mw 7.8 Kaikōura earthquake ruptured ~200 km at the ground surface across the New Zealand plate boundary zone in the northern South Island. This study was conducted in an area of ~600 km2 in the epicentral region where the faults comprise two main non-coplanar sets that strike E-NE and NNE-NW with mainly steep dips (60о-80°). Analysis of the surface rupture using field and LiDAR data provides new information on the dimensions, geometries and kinematics of these faults which was not previously available from pre-earthquake active faults or bedrock structure. The more northerly striking fault set are sub-parallel to basement bedding and accommodated predominantly left-lateral reverse slip with net slips of ~1 and ~5 m for the Stone Jug and Leader faults, respectively. The E-NE striking Conway-Charwell and The Humps faults accrued right-lateral to oblique reverse with net slips of ~2 and ~3 m, respectively. The faults form a hard-linked system dominated by kinematics consistent with the ~260° trend of the relative plate motion vector and the transpressional structures recorded across the plate boundary in the NE South Island. Interaction and intersection of the main fault sets facilitated propagation of the earthquake and transfer of slip northwards across the plate boundary zone

Fault rupture patterns during the Mw7.8 2016 Kaikoura Earthquake in the region between the Leader and Charwell rivers, north Canterbury, New Zealand

Surface rupture and slip from the Mw 7.8 2016 Kaikōura Earthquake have been mapped in the region between the Leader and Charwell rivers using field mapping and LiDAR data. The eastern Humps, north Leader and Conway-Charwell faults ruptured the ground surface in the study area. The E-NE striking ‘The Humps’ Fault runs along the base of the Mt Stewart range front, appears to dip steeply NW and intersects the NNW-NNE Leader Fault which itself terminates northwards at the NE striking Conway-Charwell Fault. The eastern Humps Fault is up to the NW and accommodates oblique slip with reverse and right lateral displacement. Net slip on ‘The Humps’ Fault is ≤4 m and produced ≤4 m uplift of the Mt Stewart range during the earthquake. The Leader Fault strikes NNW-NNE with dips ranging from ~10° west to 80° east and accommodated ≤4 m net slip comprising left-lateral and up-to-the-west vertical displacement. Like the Humps west of the study area, surface-rupture of the Leader Fault occurred on multiple strands. The complexity of rupture on the Leader Fault is in part due to the occurrence of bedding-parallel slip within the Cretaceous-Cenozoic sequence. Although the Mt Stewart range front is bounded by ‘The Humps’ Fault, in the study area neither this fault nor the Leader Fault were known to have been active before the earthquake. Fieldwork and trenching investigations are ongoing to characterise the geometry, kinematics and paleoseismic history of the mapped active faults

Measurement of in-plane elasticity of live cell layers using a pressure sensor embedded microfluidic device

[[abstract]]In various physiological activities, cells experience stresses along their in-plane direction when facing substrate deformation. Capability of continuous monitoring elasticity of live cell layers during a period is highly desired to investigate cell property variation during various transformations under normal or disease states. This paper reports time-lapsed measurement of live cell layer in-plane elasticity using a pressure sensor embedded microfluidic device. The sensor converts pressure-induced deformation of a flexible membrane to electrical signals. When cells are cultured on top of the membrane, flexural rigidity of the composite membrane increases and further changes the output electrical signals. In the experiments, human embryonic lung fibroblast (MRC-5) cells are cultured and analyzed to estimate the in-plane elasticity. In addition, the cells are treated with a growth factor to simulate lung fibrosis to study the effects of cell transformation on the elasticity variation. For comparison, elasticity measurement on the cells by atomic force microscopy (AFM) is also performed. The experimental results confirm highly anisotropic configuration and material properties of cells. Furthermore, the in-plane elasticity can be monitored during the cell transformation after the growth factor stimulation. Consequently, the developed microfluidic device provides a powerful tool to study physical properties of cells for fundamental biophysics and biomedical researches.[[notice]]補正完

Initiation factor modifications in the preapoptotic phase

Recent studies have identified several mechanistic links between the regulation of translation and the process of apoptosis. Rates of protein synthesis are controlled by a wide range of agents that induce cell death, and in many instances, the changes that occur to the translational machinery precede overt apoptosis and loss of cell viability. The two principal ways in which factors required for translational activity are modified prior to and during apoptosis involve (i) changes in protein phosphorylation and (ii) specific proteolytic cleavages. In this review, we summarise the principal targets for such regulation, with particular emphasis on polypeptide chain initiation factors eIF2 and eIF4G and the eIF4E-binding proteins. We indicate how the functions of these factors and of other proteins with which they interact may be altered as a result of activation of apoptosis and we discuss the potential significance of such changes for translational control and cell growth regulation