HEAVY-OIL PRODUCTION USING EMULSION FLOODING

In recovery of heavy crude oil by a sufficient means other than thermal recovery methods has been a great concern to researchers. Several researchers have found it difficult to achieve oil in-water (O/W) emulsion stability status. In an effort to minimize the viscosity, heavy crude needs modification.  The morphology and stability of oil-in-water emulsions were studied as a function of aqueous phase salinity. In reducing the viscosity of the heavy-oil, brine solutions were selected as alternative in forming oil-in-water (O/W) emulsion. The aim of this research is to investigate the various salinity levels that influence viscosity and stability of oil-in-water emulsion. From observation, the loose emulsions were discovered through bottle test which showed complete separation on low salinity concentration. Optical microscope assembled with a digital camera was used to investigate the oil droplets of the stable and non-stable emulsion. Results indicated that phase separation appears more easily on low concentration at room temperature, and larger size droplets in the high concentrations. Therefore, using low salinity oil in water flooding, it reduces the viscosity of heavy crude oil. http://dx.doi.org/10.4314/njt.v35i2.1

Rac1b and reactive oxygen species mediate MMP-3-induced EMT and genomic instability

5 páginas, 4 figuras.-- Letter.The tumour microenvironment can be a potent carcinogen, not only by facilitating cancer progression and activating dormant cancer cells, but also by stimulating tumour formation1. We have previously investigated stromelysin-1/matrix metalloproteinase-3 (MMP-3), a stromal enzyme upregulated in many breast tumours2, and found that MMP-3 can cause epithelial–mesenchymal transition (EMT) and malignant transformation in cultured cells3, 4, 5, and genomically unstable mammary carcinomas in transgenic mice3. Here we explain the molecular pathways by which MMP-3 exerts these effects: exposure of mouse mammary epithelial cells to MMP-3 induces the expression of an alternatively spliced form of Rac1, which causes an increase in cellular reactive oxygen species (ROS). The ROS stimulate the expression of the transcription factor Snail and EMT, and cause oxidative damage to DNA and genomic instability. These findings identify a previously undescribed pathway in which a component of the breast tumour microenvironment alters cellular structure in culture and tissue structure in vivo, leading to malignant transformation.This work was supported by grants from the OBER office of the Department of Energy and an Innovator award from the Department of Defense (to M.J.B.) and from the National Institutes of Health (to M.J.B. and Z.W.), and by fellowships from the American Cancer Society (D.C.R.), the National Cancer Institute (L.E.L.), the Department of Defense (H.L. and C.M.N.) and the California Breast Cancer Research Program (J.E.F).Peer reviewe