RESUMEN
Geological and palaeomagnetic studies indicate that ice sheets may have reached the Equator at the end of the Proterozoic eon, 800 to 550 million years ago, leading to the suggestion of a fully ice-covered 'snowball Earth'. Climate model simulations indicate that such a snowball state for the Earth depends on anomalously low atmospheric carbon dioxide concentrations, in addition to the Sun being 6 per cent fainter than it is today. However, the mechanisms producing such low carbon dioxide concentrations remain controversial. Here we assess the effect of the palaeogeographic changes preceding the Sturtian glacial period, 750 million years ago, on the long-term evolution of atmospheric carbon dioxide levels using the coupled climate-geochemical model GEOCLIM. In our simulation, the continental break-up of Rodinia leads to an increase in runoff and hence consumption of carbon dioxide through continental weathering that decreases atmospheric carbon dioxide concentrations by 1,320 p.p.m. This indicates that tectonic changes could have triggered a progressive transition from a 'greenhouse' to an 'icehouse' climate during the Neoproterozoic era. When we combine these results with the concomitant weathering effect of the voluminous basaltic traps erupted throughout the break-up of Rodinia, our simulation results in a snowball glaciation.
RESUMEN
An enigmatic chloride-rich iron (oxyhydr)oxide has been recently identified together with mercury anomalies in End-Cretaceous marine sediments coeval with the Deccan Traps eruptions. The mineral was observed in Bidart (France) and Gubbio (Italy), suggesting a widespread phenomenon. However, the exact nature and origin of this Cl-bearing mineral remained speculative. Here, we characterized the accurate composition and nanostructure of this chloride-rich phase by using micro-Raman spectroscopy, Transmission (TEM) and Scanning (SEM) Electron Microscopy on Focused Ion Beam foils. We also provide new evidence of its occurrence in Zumaia, a reference KPg section from Spain. Results confirm akaganéite (ß-FeOOH) as the main phase, with chloride content of 3-5 atomic weight %. Akaganéite particles are constituted by the aggregation of nanorods of akaganéite. Internal structures contain empty spaces, suggesting formation in a low-density (atmospheric) environment. This new mineralogical evidence supports the hypothesis that the observed akaganéite was formed in the Deccan volcanic plume and was transported to the Atlantic and Tethysian realms through the stratosphere. Therefore, akaganéite provides a potential new sedimentary marker to identify the imprint of the Deccan eruptions in the stratigraphic record and is evidence of volcanic halogen degassing and its potential role for the Cretaceous-Tertiary mass extinction.
RESUMEN
Tolerance to cerebral ischemia is achieved by preconditioning sublethal stresses, such as ischemia or hypoxia, paradigms in which the decrease of O2 availability may constitute an early signal inducing tolerance. In accordance with this concept, this study shows that hypoxia induces tolerance against focal permanent ischemia in adult mice. Normobaric hypoxia (8% O2 of 1-hour, 3-hour, or 6-hour duration), performed 24 hours before ischemia, reduces infarct volume by approximately 30% when compared with controls. To elucidate the mechanisms underlying this neuroprotection, the authors investigated the effects of preconditioning on cerebral expression of hypoxia-inducible factor-1alpha (HIF-1alpha) and its target genes, erythropoietin and vascular endothelial growth factor (VEGF). Hypoxia, whatever its duration (1 hour, 3 hours, 6 hours), rapidly increases the nuclear content of HIF-1alpha as well as the mRNA levels of erythropoietin and VEGF. Furthermore, erythropoietin and VEGF are upregulated at the protein level 24 hours after 6 hours of hypoxia. The authors' findings show that (1) hypoxia elicits a delayed, short-lasting (<72 hours) tolerance to focal permanent ischemia in the adult mouse brain; (2) HIF-1 target genes could contribute to the establishment of tolerance; and (3) this model might be a useful paradigm to further study the mechanisms of ischemic tolerance, to identify new therapeutic targets for stroke.