Irregular rupture process of the 2022 Taitung, Taiwan, earthquake sequence.

In September 2022, two destructive earthquakes of moment magnitude (Mw) 6.6 (foreshock) and 7.1 (mainshock) occurred in Taitung County, south-eastern Taiwan. To understand their complex rupture processes, we analysed these earthquakes using the Potency Density Tensor Inversion method, which can stably estimate the rupture propagation process, including fault geometry, without overfitting the data. The analyses revealed that the major rupture of the foreshock propagated towards shallow depth, in a south-southwest direction, following an initial rupture that propagated towards the deeper part of the fault. The mainshock, with its epicentre on the north-northeast side of that of the foreshock, consists of two distinct episodes. During the first episode (0-10 s), the initial rupture propagated north-northeast, through a deep path, followed by the main rupture that propagated bilaterally in a north-northeast and south-southwest direction. The second rupture episode (10-16 s) started near the hypocentre of the mainshock, and the rupture propagated towards the shallow side of the fault. The results suggest that the stress concentration from both the foreshock and mainshock's first rupture episode may have caused the second rupture episode in the high fracture surface energy area between the foreshock and the first rupture episode of the mainshock. The irregular rupture process of the foreshock and mainshock may reflect the heterogeneity of stress and structure in the source region.

Irregular rupture propagation and geometric fault complexities during the 2010 Mw 7.2 El Mayor-Cucapah earthquake.

The 2010 MW 7.2 El Mayor-Cucapah, Mexico, earthquake ruptured multiple faults with different faulting mechanisms. Resolving the earthquake rupture process and its relation to the geometric fault complexities is critical to our understanding of the earthquake source physics, but doing so by conventional finite-fault inversion is challenging because modelling errors due to inappropriate assumptions about the fault geometry distort the solution and make robust interpretation difficult. Here, using a potency density tensor approach to finite-fault inversion, we inverted the observed teleseismic P waveforms of the 2010 El Mayor-Cucapah earthquake to simultaneously estimate the rupture process and the fault geometry. We found that the earthquake consisted of an initial normal faulting rupture, which was followed by a strike-slip bilateral rupture towards the southeast and northwest that originated on the northwest side of the epicentre. The southeastern rupture propagated back through the initial rupture area, but with strike-slip faulting. Although the northwestern rupture propagated across the left step in the Puerta fault-accommodation zone, the rupture was temporarily stalled by the associated change of the fault geometry. These results highlight the irregular rupture process, which involved a back-propagating rupture and fluctuating rupture propagation controlled the complexity of the fault system.

Consecutive ruptures on a complex conjugate fault system during the 2018 Gulf of Alaska earthquake.

We developed a flexible finite-fault inversion method for teleseismic P waveforms to obtain a detailed rupture process of a complex multiple-fault earthquake. We estimate the distribution of potency-rate density tensors on an assumed model plane to clarify rupture evolution processes, including variations of fault geometry. We applied our method to the 23 January 2018 Gulf of Alaska earthquake by representing slip on a projected horizontal model plane at a depth of 33.6 km to fit the distribution of aftershocks occurring within one week of the mainshock. The obtained source model, which successfully explained the complex teleseismic P waveforms, shows that the 2018 earthquake ruptured a conjugate system of N-S and E-W faults. The spatiotemporal rupture evolution indicates irregular rupture behavior involving a multiple-shock sequence, which is likely associated with discontinuities in the fault geometry that originated from E-W sea-floor fracture zones and N-S plate-bending faults.

Relationship between high-frequency radiation and asperity ruptures, revealed by hybrid back-projection with a non-planar fault model.

High-frequency seismic waves are generated by abrupt changes of rupture velocity and slip-rate during an earthquake. Therefore, analysis of high-frequency waves is crucial to understanding the dynamic rupture process. Here, we developed a hybrid back-projection method that considers variations in focal mechanisms by introducing a non-planar fault model that reflects the subducting slab geometry. We applied it to teleseismic P-waveforms of the Mw 8.8 2010 Chile earthquake to estimate the spatiotemporal distribution of high-frequency (0.5-2.0 Hz) radiation. By comparing the result with the coseismic slip distribution obtained by waveform inversion, we found that strong high-frequency radiation can precede and may trigger a large asperity rupture. Moreover, in between the large slip events, high-frequency radiation of intermediate strength was concentrated along the rupture front. This distribution suggests that by bridging the two large slips, this intermediate-strength high-frequency radiation might play a key role in the interaction of the large slip events.

A pitfall in diagnosis of human prion diseases using detection of protease-resistant prion protein in urine. Contamination with bacterial outer membrane proteins.

Because a definite diagnosis of prion diseases relies on the detection of the abnormal isoform of prion protein (PrPSc), it has been urgently necessary to establish a non-invasive diagnostic test to detect PrPSc in human prion diseases. To evaluate diagnostic usefulness and reliability of the detection of protease-resistant prion protein in urine, we extensively analyzed proteinase K (PK)-resistant proteins in patients affected with prion diseases and control subjects by Western blot, a coupled liquid chromatography and mass spectrometry analysis, and N-terminal sequence analysis. The PK-resistant signal migrating around 32 kDa previously reported by Shaked et al. (Shaked, G. M., Shaked, Y., Kariv-Inbal, Z., Halimi, M., Avraham, I., and Gabizon, R. (2001) J. Biol. Chem. 276, 31479-31482) was not observed in this study. Instead, discrete protein bands with an apparent molecular mass of approximately 37 kDa were detected in the urine of many patients affected with prion diseases and two diseased controls. Although these proteins also gave strong signals in the Western blot using a variety of anti-PrP antibodies as a primary antibody, we found that the signals were still detectable by incubation of secondary antibodies alone, i.e. in the absence of the primary anti-PrP antibodies. Mass spectrometry and N-terminal protein sequencing analysis revealed that the majority of the PK-resistant 37-kDa proteins in the urine of patients were outer membrane proteins (OMPs) of the Enterobacterial species. OMPs isolated from these bacteria were resistant to PK and the PK-resistant OMPs from the Enterobacterial species migrated around 37 kDa on SDS-PAGE. Furthermore, nonspecific binding of OMPs to antibodies could be mistaken for PrPSc. These findings caution that bacterial contamination can affect the immunological detection of prion protein. Therefore, the presence of Enterobacterial species should be excluded in the immunological tests for PrPSc in clinical samples, in particular, urine.