Description: Spreading is a common type of ground failure in subaerial environments. However, this type of mass movement has hardly been documented in submarine settings. In this paper we show that spreading covers at least 25% of the Storegga Slide scar area, a giant submarine slide located offshore mid-Norway. The morphological signature of spreading is a repetitive pattern of ridges and troughs oriented perpendicular to the direction of movement. Two modes of failure can be identified: retrogressive failure of the headwall and slab failure and extension, both involving the breakup of a sediment unit into coherent blocks. These blocks are displaced downslope along planar slip surfaces. Limit equilibrium modeling indicates that loss of support and seismic loading are the main potential triggering mechanisms. The extent of displacement of the spreading sediment is controlled by gravitationally induced stress, angle of internal friction of the sediment, pore pressure escape, and friction. The resulting block movement pattern entails an exponential increase of displacement and thinning of the failing sediment with distance downslope. Sediment properties explain the remaining spatial variation of ridge and trough morphologies associated with spreading.

Description: In comparison to subaerial and planetary landscapes, submarine environments are rarely investigated using quantitative geomorphological techniques. Application of traditional geomorphometric techniques is hindered by the spatial variability in bathymetric data resolution and the extensive scale over which changes in topography occur. We propose a novel methodology for the improved quantitative analysis of submarine elevation data by adapting numerical techniques, developed for subaerial analyses, to submarine environments. The method integrates three main morphometric techniques: (1) morphometric attributes and their statistical analyses, (2) feature-based quantitative representation, and (3) automated topographic classification. These techniques allow useful morphological information to be extracted from a digital elevation model. Morphometric attributes and their statistical analyses provide summary information about an area, which can be used to calibrate computer-generated geomorphometric maps. In these maps the boundaries of geomorphological features are delineated, and they can thus be used as the basis for geomorphological interpretation. Ridge patterns and their morphological characteristics provide an accurate representation of specific aspects of terrain variability. Moment statistics are used as proxies of surface roughness to differentiate between surface types. Unsupervised classification, carried out using ridge characteristics and moment statistics, reliably segments the surface into units of homogeneous topography. A case study of debris flow lobes within the Storegga Slide shows that the techniques work robustly and that the new methodology integrating all the techniques can significantly enhance submarine geomorphological investigations.

Description: Objective— Liver X receptors (LXRs) are oxysterol-activated nuclear receptors that are highly expressed in macrophages and regulate lipid homeostasis and inflammation. Among putative LXR target genes, lysophosphatidylcholine acyltransferase 3 (LPCAT3) involved in the Lands cycle controls the fatty acid composition at the sn-2 position of glycerophospholipids and, therefore, the availability of fatty acids, such as arachidonic acid (AA), used for eicosanoid synthesis. The aim of our study was to determine whether LXRs could regulate the Lands cycle in human macrophages, to assess the consequences in terms of lipid composition and inflammatory response, and to work out the relative contribution of LPCAT3 to the observed changes. Approach and Results— Transcriptomic analysis revealed that LPCAT3 was upregulated by LXR agonists in human macrophages. Accordingly, LXR stimulation significantly increased lysophospholipid acyltransferase activity catalyzed by LPCAT3. Lipidomic analysis demonstrated that LXR activation increased the AA content in the polar lipid fraction, specifically in phosphatidylcholines. The LXR-mediated effects on AA distribution were abolished by LPCAT3 silencing, and a redistribution of AA toward the neutral lipid fraction was observed in this context. Finally, we observed that preconditioning of human macrophages by LXR agonist treatment increased the release of arachidonate-derived eicosanoids, such as prostaglandin E 2 and thromboxane after lipopolysaccharide stimulation, with a significant attenuation by LPCAT3 silencing. Conclusions— Altogether, our data demonstrate that the LXR-mediated induction of LPCAT3 primes human macrophages for subsequent eicosanoid secretion by increasing the pool of AA, which can be mobilized from phospholipids.

Description: Large-scale landslides occur on the flanks of many volcanic oceanic islands worldwide. None have taken place in historical time, but their geohazard potential, especially their ability to generate tsunamis, is large. The Cape Verde Islands are a group of 10 large and several smaller volcanic islands off the coast of West Africa between 15 and 17°N. A single flank landslide has previously been described from the island of Fogo, but systematic analysis of the Cape Verde group has until now been lacking. This paper describes and interprets a multibeam bathymetry data set covering the slopes of the western Cape Verde Islands, including those of the islands with the most recent volcanic activity, Fogo in the southwest, and Santo Antao in the northwest. All of the larger islands show evidence of large flank landslides, although only Fogo and the southwest part of Santo Antao have failed in the last 400 ka. Tope de Coroa, the volcano at the southwest end of Santo Antao, has been inactive for the past 170 ka and is judged to have a low landslide potential unless volcanic activity resumes. In contrast, there would seem to be a high probability of a future east directed landslide on Fogo, from the area of the highly active Pico do Fogo volcano, although it is impossible to predict a timescale for such an event. A tsunami generated by such a landslide could have a catastrophic effect on the adjacent island of Santiago and possibly even farther afield on the West African coast.

Description: Objective— Liver X receptors (LXRs) modulate cholesterol and fatty acid homeostasis as well as inflammation. This study aims to decipher the role of LXRs in the regulation of polyunsaturated fatty acid (PUFA) synthesis in macrophages in the context of atherosclerosis. Approach and Results— Transcriptomic analysis in human monocytes and macrophages was used to identify putative LXR target genes among enzymes involved in PUFA biosynthesis. In parallel, the consequences of LXR activation or LXR invalidation on PUFA synthesis and distribution were determined. Finally, we investigated the impact of LXR activation on PUFA metabolism in vivo in apolipoprotein E–deficient mice. mRNA levels of acyl-CoA synthase long-chain family member 3, fatty acid desaturases 1 and 2, and fatty acid elongase 5 were significantly increased in human macrophages after LXR agonist treatment, involving both direct and sterol responsive element binding protein-1–dependent mechanisms. Subsequently, pharmacological LXR agonist increased long chain PUFA synthesis and enhanced arachidonic acid content in the phospholipids of human macrophages. Increased fatty acid desaturases 1 and 2 and acyl-CoA synthase long-chain family member 3 mRNA levels as well as increased arachidonic acid to linoleic acid and docosahexaenoic acid to eicosapentaenoic acid ratios were also found in atheroma plaque and peritoneal foam cells from LXR agonist–treated mice. By contrast, murine LXR-deficient macrophages displayed reduced expression of fatty acid elongase 5, acyl-CoA synthase long-chain family member 3 and fatty acid desaturases 1, as well as decreased cellular levels of docosahexaenoic acid and arachidonic acid. Conclusions— Our results indicate that LXR activation triggers PUFA synthesis in macrophages, which results in significant alterations in the macrophage lipid composition. Moreover, we demonstrate here that LXR agonist treatment modulates PUFA metabolism in atherosclerotic arteries.