Relative rates of fluid advection, elemental diffusion and replacement govern reaction front patterns

Replacement reactions during fluid infiltration into porous media, rocks and buildings are known to have important implications for reservoir development, ore formation as well as weathering. Natural observations and experiments have shown that in such systems the shape of reaction fronts can vary significantly ranging from smooth, rough to highly irregular. It remains unclear what process-related knowledge can be derived from these reaction front patterns. In this contribution we show a numerical approach to test the effect of relative rates of advection, diffusion, and reaction on the development of reaction fronts patterns in granular aggregates with permeable grain boundaries. The numerical model takes (i) fluid infiltration along permeable grain boundaries, (ii) reactions and (iii) elemental diffusion into account. We monitor the change in element concentration within the fluid, while reactions occur at a pre-defined rate as a function of the local fluid concentration. In non-dimensional phase space using Péclet and Damköhler numbers, results show that there are no rough fronts without advection (Péclet10−3). As advection becomes more dominant and reaction slower, roughness develops across several grains with a full microstructure mimicking replacement in the most extreme cases. The reaction front patterns show an increase in roughness with increasing Péclet number from Péclet 10 to 100 but then a decrease in roughness towards higher Péclet numbers controlled by the Damköhler number. Our results indicate that reaction rates are crucial for pattern formation and that the shape of reaction fronts is only partly due to the underlying transport mechanism

Avicin D: A Protein Reactive Plant Isoprenoid Dephosphorylates Stat 3 by Regulating Both Kinase and Phosphatase Activities

Avicins, a class of electrophilic triterpenoids with pro-apoptotic, anti-inflammatory and antioxidant properties, have been shown to induce redox-dependant post-translational modification of cysteine residues to regulate protein function. Based on (a) the cross-talk that occurs between redox and phosphorylation processes, and (b) the role of Stat3 in the process of apoptosis and carcinogenesis, we chose to study the effects of avicins on the processes of phosphorylation/dephosphorylation in Stat3. Avicins dephosphorylate Stat3 in a variety of human tumor cell lines, leading to a decrease in the transcriptional activity of Stat3. The expression of Stat3-regulated proteins such as c-myc, cyclin D1, Bcl2, survivin and VEGF were reduced in response to avicin treatment. Underlying avicin-induced dephosphorylation of Stat3 was dephosphorylation of JAKs, as well as activation of protein phosphatase-1. Downregulation of both Stat3 activity and expression of Stat 3-controlled pro-survival proteins, contributes to the induction of apoptosis in avicin treated tumor cells. Based on the role of Stat3 in inflammation and wounding, and the in vivo inhibition of VEGF by avicins in a mouse skin carcinogenesis model, it is likely that avicin-induced inhibition of Stat3 activity results in the suppression of the pro-inflammatory and pro-oxidant stromal environment of tumors. Activation of PP-1, which also acts as a cellular economizer, combined with the redox regulation by avicins, can aid in redirecting metabolism from growth promoting anabolic to energy sparing pathways