The mechanical impact of CO2 injection

The mechanical impact of CO2 injection into a depleted hydrocarbon field or aquifer is caused by changes in the stress field, resulting from changes in the pore pressure and volume of the rock. Mechanical processes can lead to the loss of reservoir and caprock integrity, and the reactivation of existing faults. A geomechanical numerical modelling approach to determining the mechanical impact of CO2 injection is presented and demonstrated on two sites studied as part of the European Community funded project 'Natural Analogues for the storage of CO2 in the Geological Environment' (NASCENT)

Monitoring Subsurface CO

An overview is given of various currently applied monitoring techniques for CO2 storage. Techniques are subdivided in correspondence to their applicability for monitoring three distinct realms. These are: - the atmosphere and the near- surface; - the overburden (including faults and wells); - the reservoir with its seals. Another subdivision can be made with respect to time, i.e. first monitoring during the injection and storage process and subsequently monitoring for the long term (after abandonment of the field). In this perspective, the importance of characterisation and monitoring before injection is addressed

Soy extract has different effects compared with the isolated isoflavones on the proteome of homocysteine-stressed endothelial cells

Epidemiological studies suggest that soy consumption may provide a protection in the development and progression of atherosclerosis. It is under debate, however, whether the soy isoflavones or other compounds are the active principle. As apoptosis is a driving force in the process of atherosclerosis, we tested whether a soy extract or a combination of the two predominant isoflavones genistein and daidzein, in concentrations as found in the extract, exert similar or different effects on apoptosis in EA.hy 926 endothelial cells after exposure to the endothelial stressor homocysteine. Plasma membrane disintegration and nuclear fragmentation served as relevant apoptosis markers. To assess whether the extract and the genistein/daidzein mixture differently affect cellular target proteins changed in amount by homocysteine treatment, proteome analysis was performed by two-dimensional gel-electrophoresis and peptide mass fingerprinting of regulated protein spots. Homocysteine induced apoptosis in the cells, and both extract and genistein/daidzein inhibited apoptosis to a comparable extent. Whereas the extract prevented for 10 proteins the changes in expression levels as caused by homocysteine, the genistein/daidzein mixture reversed the homocysteine effects on the proteome for 13 proteins. The cytoskeletal protein matrin 3 and a U5 snRNP-specific 40-kDa protein were the only protein entities where both extract and genistein/daidzein reversed the homocysteine-induced changes in a common way. In conclusion, our studies provide evidence that an isoflavone containing soy extract and isolated isoflavones, despite similar effects on inhibition of homocysteine-induced apoptosis in endothelial cells, affect a quite different spectrum of cellular target proteins

Proteome analysis suggests that mitochondrial dysfunction in stressed endothelial cells is reversed by a soy extract and isolated isoflavones

Apoptosis is a driving force in atherosclerosis development. A soy extract or a combination of the soy isoflavones genistein and daidzein inhibited apoptosis induced by oxidized LDL in endothelial cells. Proteome analysis revealed that the LDL-induced alterations of numerous proteins were reversed by the extract and the genistein/daidzein mixture but only three protein entities, all functionally linked to mitochondrial dysfunction, were regulated in common by both treatments