Kaolin polytype evidence for a hot-fluid pulse along Caledonian thrusts during rifting of the European Margin

Sedimentary basins developed along the European margin during the earliest, Permian, stage of proto-Atlantic rifting, during a phase of high heat flow. The proximity of some basins to Caledonian thrusts has implied that rifts locally utilized the basement fabric. New mineralogical and palaeomagnetic data show that thrust planes in the Moine Thrust Zone channelled a Pulse of hot fluid in Permian time. The fluids precipitated kaolin in fractures in the thrust zone, and with decreasing intensity away from the zone. The high-temperature polytype dickite is largely confined to major thrust planes. Stable H and 0 isotope analyses indicate that the parent fluid included meteoric water involved in a hydrothermal system. Coeval hydrothermal hematite has a chemical remanence that dates the fluid pulse as Permian. This is direct evidence for post-orogenic activity in the thrust zone, in which the thrusts vented excess heat during regional crustal extension. The example from the European margin exemplifies the importance of deep-seated structures in the release of heat, and the value of kaolinite polytype mapping as a toot to record anomalous palaeo-heat flow

Mitochondrial targeting by use of lipid nanocapsules loaded with SV30, an analogue of the small-molecule Bcl-2 inhibitor HA14-1.

International audienceTaking advantage from the development of SV30, a new analogue of the pro-apoptotic molecule HA14-1, the aim of this study was to functionally evaluate SV30 and to develop safe nanocarriers for its administration. By using an inversion phase process, 57nm organic solvent-free lipid nanocapsules loaded with SV30 (SV30-LNCs) were formulated. Biological performance of SV30 and SV30-LNCs were evaluated on F98 cells that express Bax and Bcl-2, through survival assays, HPLC, flow cytometry, confocal microscopy and spectral imaging. We observed that SV30 alone or in combination with paclitaxel, etoposide or beam radiation could trigger cell death in a similar fashion to HA14-1. Although partially blocked by Z-VAD-fmk, this effect was coincident to caspase-3 activation. Hence, we established that SV30-LNCs improved SV30 biological activity together with a potentiation of the mitochondrial membrane potential decrease. Interestingly, flow cytometry and confocal analysis indicated that SV30 itself conferred to LNCs improved mitochondrial targeting skills that may present a great interest toward the development of mitochondria targeted nanomedicines