[1] We use 50 Tonga-Fiji events recorded at the broadband TriNet array, southern California, to develop a pure path upper mantle shear velocity model across the Pacific. At the epicentral distances of 70°-95°, multibounce S waves up to S 5 are observed, including their triplicated branches, which become particularly clear after stacking. Since these S wave multiples turn at various depths, simultaneously modeling their differential traveltimes and waveforms provides strong constraints on the radial velocity structure. We parameterize the velocity model according to a priori information from the previous oceanic models, so that we can take a grid search approach, to fully investigate possible interdependencies among the model parameters. We construct synthetics with a reflectivity code and study both the SH and SV components. By modeling the whole recordings from events at different depths, with different mechanisms, we are able to separate shallow low-velocity zone (LVZ) features from deeper structure. Our preferred model (PAC06) contains a fast lid (V sh = 4.78 km s À1 , V sv = 4.58 km s À1 ) with a thickness of $60 km. The underlying LVZ is prominent with the lowest velocities V sh = 4.34 km s À1 , and V sv = 4.22 km s À1 occurring at a depth of $160 km. These velocities are below the estimates of solid-state LVZ, suggesting the presence of partial melt. The anisotropy (V sv < V sh ) of PAC06 extends to $300 km depth, which is constrained by S 5 turning at this depth. Besides the 406 km and 651 km discontinuities, PAC06 also has a small ($1%) velocity jump at $516 km. We consider these main features of PAC06 to be well determined, since PAC06 explains a large data set from various events. Therefore it is ideally suited for comparing with mineralogical models.
[1] The slip history of the 2003 San Simeon earthquake is constrained by combining strong motion and teleseismic data, along with GPS static offsets and 1-Hz GPS observations. Comparisons of a 1-Hz GPS time series and a co-located strong motion data are in very good agreement, demonstrating a new application of GPS. The inversion results for this event indicate that the rupture initiated at a depth of 8.5 km and propagated southeastwards with a speed $3.0 km/sec, with rake vectors forming a fan structure around the hypocenter. We obtained a peak slip of 2.8 m and total seismic moment of 6.2 Â 10 18 Nm. We interpret the slip distribution as indicating that the hanging wall rotates relative to the footwall around the hypocenter, in a sense that appears consistent with the shape of the mapped fault trace.
[1] We developed a new technique CAPloc to retrieve full source parameters of small seismic events from regional seismograms, which include origin time, epicenter location, depth, focal mechanism, and moment magnitude. Despite rather complicated propagation effects at short periods, a simple localized one-dimensional model can well explain signals of periods 3-10 s if we break the three-component records into different segments and allow differential time shifts among them. These differential time shifts, once established from a calibration process or a well-determined tomographic map, can be used together with P wave travel times to refine an event's location. In this study, we tested whether our new method could produce satisfactory results with as few as two stations, so that we can improve source estimates of poorly monitored events with sparse waveform data. We conducted the test on 28 events in the Tibetan Plateau. The focal mechanisms and locations determined from only two stations agree well with those determined from a whole PASSCAL array. In particular, our new method produces better locations than International Seismological Centre, with the average mislocation error reduced from $16 to $5 km. We also tested whether an event's depth and mechanism can be determined separately from its epicenter relocation in a two-step approach. We find that the two-step approach does not always give the correct solution, but the reliability of a solution can be evaluated using a reduced chi-square value.
Cellular stress or injury induces release of endogenous danger signals such as ATP, which plays a central role in activating immune cells. ATP is essential for the release of nonclassically secreted cytokines such as IL-1β but, paradoxically, has been reported to inhibit the release of classically secreted cytokines such as TNF. Here, we reveal that ATP does switch off soluble TNF (17 kDa) release from LPS-treated macrophages, but rather than inhibiting the entire TNF secretion, ATP packages membrane TNF (26 kDa) within microvesicles (MVs). Secretion of membrane TNF within MVs bypasses the conventional endoplasmic reticulum– and Golgi transport–dependent pathway and is mediated by acid sphingomyelinase. These membrane TNF–carrying MVs are biologically more potent than soluble TNF in vivo , producing significant lung inflammation in mice. Thus, ATP critically alters TNF trafficking and secretion from macrophages, inducing novel unconventional membrane TNF signaling via MVs without direct cell-to-cell contact. These data have crucial implications for this key cytokine, particularly when therapeutically targeting TNF in acute inflammatory diseases.—Soni, S., O’Dea, K. P., Tan, Y. Y., Cho, K., Abe, E., Romano, R., Cui, J., Ma, D., Sarathchandra, P., Wilson, M. R., Takata, M. ATP redirects cytokine trafficking and promotes novel membrane TNF signaling via microvesicles.
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