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A fully operational system would use a network of sensors — 300 are in place now, but hundreds more are needed — to detect the first signs of a rupture, using the data to project the severity and breadth of the quake, the area most likely to be damaged and the number of seconds until the shaking begins.
Yagi et al. (2016) reveal the temporal evolution of rupture using seismograms from a global network.
Previous studies illuminated the complexity of the 2016 Mw 7.8 multi-fault rupture using geodetic, seismological, and geological observations.
We investigated the effects of heterogeneous crustal structure on earthquake rupture, using the 2004 Chuetsu earthquake and its source region as a case study.
Figure 1 shows the location of rupture using data of Peak Ground Velocity according the Finite Fault Model calculate by Ji and Hayes (2008).
We nucleate the rupture using the time-weakening procedure of Andrews (1985) with an imposed rupture speed of 800 m/s.
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Participants were excluded if they had: a previous Achilles tendon rupture; used medication known to affect tendons in the previous 3 months (e.g. fluroquinolone antibiotics, corticosteroids); inflammatory conditions such as ankylosing spondylitis, rheumatoid arthritis and related conditions; or were under the age of 18.
The same suspension was ruptured using sufficient volume of ethanol, and the total amount of EGCG was determined spectrophotometrically.
The same suspension was ruptured using sufficient volume of ethanol, and the total amount of Lf was determined spectrophotometrically.
Goto et al. (2017) examine subtle geomorphic features of surface ruptures using a digital elevation model in the city of Kumamoto and discuss their possible relationship to the earthquake source faults.
No activity was observed when the mitochondria were incubated with an RNA substrate in the isotonic buffer, but the RNA substrate was quickly degraded when the outer membrane was ruptured using hypotonic buffer, suggesting the outer surface of the purified mitochondria harbors no ribonuclease activity and the IMS activity has no cytosolic contamination (Fig. 2C).
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