Holocene tectonic, sedimentary, and erosive processes in a volcanic-dammed intramontane lacustrine basin: Lago Laja, Chile

Lago Laja is located near the drainage divide of the south-central high Andes at 37°S. The active Antuco volcano, adjacent to the lake, forms a natural dam confining the Laja intramontane basin. We use field observations, lake reflection-seismic profiles, bathymetry, and remote sensing data to reconstruct the late Quaternary erosion and sedimentation history of the Laja basin and to document the existence of an active fault system that runs parallel to the volcanic arc, the Lago Laja fault system (LLFS).Activity of the Antuco volcano started at ~124 ka with formation of the basaltic edifice, which dammed the catchments forming the intramone Laja basin and lake. At 7.1 cal ka BP, a caldera-collapse event of the Antuco opened the Laja’s dam generating an outburst megaflood and emptying the lake. Fluvial systems advanced into the former lake eroding the poorly-consolidated lacustrine sediments. Subsequent Late Holocene post-caldera lavas dammed the Laja’s outflow generating the present-day lake and renewed lacustrine sedimentation. The fluvial erosion episode is recorded in a regional unconformity, which is well observed in seismic profiles and thus represents an excellent structural marker to quantify fault activity. A post-7.1 ka lacustrine drape covers the erosional surface.Normal faults of the LLFS cut the -14 s-1. Pyroclastic deposits of the Chillan volcano in the northern segment yield a vertical slip rate of 1.0 ± 0.05 mm/a.We interpret soft-sediment deformation layers in an exposed late Pleistocene glaciolacustrine sequence as seismites, which evidence M>6 paleoearthquakes. This is in agreement with magnitudes expected from Holocene surface ruptures.The Main Cordillera at ~37°S is a large-scale pop-up structure uplifted by Quaternary thrusting along both its foothills. In this light, we interpret extension in the axial and highest part of the Andes as incipient gravitational collapse in response to surface uplift and crustal thickening. Thermal weakening due to elevated heat flow in the vicinity of the volcanic arc and post-glacial lithospheric rebound have probably contributed to the arc-limited collapse and late Quaternary acceleration of deformation rates

Amphibious Seismic Survey Images Plate Interface at 1960 Chile Earthquake

The southern central Chilean margin at the site of the largest historically recorded earthquake in the Valdivia region, in 1960 (Mw = 9.5), is part of the 5000-km-long active subduction system whose geodynamic evolution is controversially debated and poorly understood. Covering the area between 36° and 40°S, the oceanic crust is segmented by prominent fracture zones. The offshore forearc and its onshore continuation show a complex image with segments of varying geophysical character, and several fault systems active during the past 24 m.y. In autumn 2001, the project SPOC was organized to study the Subduction Processes Off Chile, with a focus on the seismogenic coupling zone and the forearc. The acquired seismic data crossing the Chilean subduction system were gathered in a combined offshore-onshore survey and provide new insights into the lithospheric structure and evolution of active margins with insignificant frontal accretion

The Use of Spinning-Disk Confocal Microscopy for the Intravital Analysis of Platelet Dynamics in Response to Systemic and Local Inflammation

Platelets are central players in inflammation and are an important component of the innate immune response. The ability to visualize platelets within the live host is essential to understanding their role in these processes. Past approaches have involved adoptive transfer of labelled platelets, non-specific dyes, or the use of fluorescent antibodies to tag platelets in vivo. Often, these techniques result in either the activation of the platelet, or blockade of specific platelet receptors. In this report, we describe two new methods for intravital visualization of platelet biology, intravenous administration of labelled anti-CD49b, which labels all platelets, and CD41-YFP transgenic mice, in which a percentage of platelets express YFP. Both approaches label endogenous platelets and allow for their visualization using spinning-disk confocal fluorescent microscopy. Following LPS-induced inflammation, we were able to measure a significant increase in both the number and size of platelet aggregates observed within the vasculature of a number of different tissues. Real-time observation of these platelet aggregates reveals them to be large, dynamic structures that are continually expanding and sloughing-off into circulation. Using these techniques, we describe for the first time, platelet recruitment to, and behaviour within numerous tissues of the mouse, both under control conditions and following LPS induced inflammation

Platelet GPIIb supports initial pulmonary retention but inhibits subsequent proliferation of melanoma cells during hematogenic metastasis

Platelets modulate the process of cancer metastasis. However, current knowledge on the direct interaction of platelets and tumor cells is mostly based on findings obtained in vitro. We addressed the role of the platelet fibrinogen receptor glycoprotein IIb (integrin alpha IIb) for experimental melanoma metastasis in vivo. Highly metastatic B16-D5 melanoma cells were injected intravenously into GPIIb-deficient (GPIIb(-/-)) or wildtype (WT) mice. Acute accumulation of tumor cells in the pulmonary vasculature was assessed in real-time by confocal videofluorescence microscopy. Arrest of tumor cells was dramatically reduced in GPIIb(-/-) mice as compared to WT. Importantly, we found that mainly multicellular aggregates accumulated in the pulmonary circulation of WT, instead B16-D5 aggregates were significantly smaller in GPIIb(-/-) mice. While pulmonary arrest of melanoma was clearly dependent on GPIIb in this early phase of metastasis, we also addressed tumor progression 10 days after injection. Inversely, and unexpectedly, we found that melanoma metastasis was now increased in GPIIb(-/-) mice. In contrast, GPIIb did not regulate local melanoma proliferation in a subcutaneous tumor model. Our data suggest that the platelet fibrinogen receptor has a differential role in the modulation of hematogenic melanoma metastasis. While platelets clearly support early steps in pulmonary metastasis via GPIIb-dependent formation of platelet-tumor-aggregates, at a later stage its absence is associated with an accelerated development of melanoma metastases