Detection of the 2010 Chilean Tsunami Using Satellite Altimetry

Tsunamis are difficult to detect and measure in the open ocean because the wave amplitude is much smaller than it is closer to shore. An effective early warning system, however, must be able to observe an impending tsunami threat far away from the shore in order to provide the necessary lead-time for coastal inhabitants to find safety. Given the expansiveness of the ocean, sensors capable of detecting the tsunami must also have very broad areal coverage. The 2004 Sumatra-Andaman tsunami was definitively detected in the open ocean from both sea surface height and sea surface roughness measurements provided by satellite altimeters. This tsunami, however, was exceptionally strong and questions remain about the ability to use such measurements for the detection of weaker tsunamis. Here we study the 2010 Chilean tsunami and demonstrate the ability to detect the tsunami in the open ocean. Specifically, we analyze the utility of filtering in extracting the tsunami signal from sea surface height measurements, and, through the use of statistical analyses of satellite altimeter observations, we demonstrate that the 2010 Chilean tsunami induced distinct and detectable changes in sea surface roughness. While satellite altimeters do not provide the temporal and spatial coverage necessary to form the basis of an effective early warning system, tsunami-induced changes in sea surface roughness can be detected using orbiting microwave radars and radiometers, which have a broad surface coverage across the satellite ground track

Variations in sea surface roughness induced by the 2004 Sumatra-Andaman tsunami

Observations of tsunamis away from shore are critically important for improving early warning systems and understanding of tsunami generation and propagation. Tsunamis are difficult to detect and measure in the open ocean because the wave amplitude there is much smaller than it is close to shore. Currently, tsunami observations in deep water rely on measurements of variations in the sea surface height or bottom pressure. Here we demonstrate that there exists a different observable, specifically, ocean surface roughness, which can be used to reveal tsunamis away from shore. The first detailed measurements of the tsunami effect on sea surface height and radar backscattering strength in the open ocean were obtained from satellite altimeters during passage of the 2004 Sumatra-Andaman tsunami. Through statistical analyses of satellite altimeter observations, we show that the Sumatra-Andaman tsunami effected distinct, detectable changes in sea surface roughness. The magnitude and spatial structure of the observed variations in radar backscattering strength are consistent with hydrodynamic models predicting variations in the near-surface wind across the tsunami wave front. Tsunami-induced changes in sea surface roughness can be potentially used for early tsunami detection by orbiting microwave radars and radiometers, which have broad surface coverage across the satellite ground track

Could Satellite Altimetry Have Improved Early Detection and Warning of the 2011 Tohoku Tsunami?

The 2011 Tohoku tsunami devastated Japan and affected coastal populations all around the Pacific Ocean. Accurate early warning of an impending tsunami requires the detection of the tsunami in the open ocean. While the lead-time was not sufficient for use in warning coastal populations in Japan, satellite altimetry observations of the tsunami could have been used to improve predictions and warnings for other affected areas. By comparing to both model results and historical satellite altimeter data, we use near-real-time satellite altimeter measurements to demonstrate the potential for detecting the 2011 Tohoku tsunami within a few hours of the tsunami being generated. We show how satellite altimeter data could be used to both directly detect tsunamis in the open ocean and also improve predictions made by models

Longitudinal intravital imaging of the retina reveals long-term dynamics of immune infiltration and its effects on the glial network in experimental autoimmune uveoretinitis, without evident signs of neuronal dysfunction in the ganglion cell layer

A hallmark of autoimmune retinal inflammation is the infiltration of the retina with cells of the innate and adaptive immune system, leading to detachment of the retinal layers and even to complete loss of the retinal photoreceptor layer. As the only optical system in the organism, the eye enables non-invasive longitudinal imaging studies of these local autoimmune processes and of their effects on the target tissue. Moreover, as a window to the central nervous system (CNS), the eye also reflects general neuroinflammatory processes taking place at various sites within the CNS. Histological studies in murine neuroinflammatory models, such as experimental autoimmune uveoretinitis (EAU) and experimental autoimmune encephalomyelitis, indicate that immune infiltration is initialized by effector CD4(+) T cells, with the innate compartment (neutrophils, macrophages, and monocytes) contributing crucially to tissue degeneration that occurs at later phases of the disease. However, how the immune attack is orchestrated by various immune cell subsets in the retina and how the latter interact with the target tissue under in vivo conditions is still poorly understood. Our study addresses this gap with a novel approach for intravital two-photon microscopy, which enabled us to repeatedly track CD4(+) T cells and LysM phagocytes during the entire course of EAU and to identify a specific radial infiltration pattern of these cells within the inflamed retina, starting from the optic nerve head. In contrast, highly motile [Formula: see text] cells display an opposite radial motility pattern, toward the optic nerve head. These inflammatory processes induce modifications of the microglial network toward an activated morphology, especially around the optic nerve head and main retinal blood vessels, but do not affect the neurons within the ganglion cell layer. Thanks to the new technology, non-invasive correlation of clinical scores of CNS-related pathologies with immune infiltrate behavior and subsequent tissue dysfunction is now possible. Hence, the new approach paves the way for deeper insights into the pathology of neuroinflammatory processes on a cellular basis, over the entire disease course