Stability and performance enhancements of Electrokinetic-Fenton soil remediation

Electrokinetic process is a potential in situ soil remediation process which transports the contaminants via electromigration and electroosmosis. For organic compounds contaminated soil, Fenton’s reagent is utilized as a flushing agent in electrokinetic process (Electrokinetic-Fenton) so that removal of organic contaminants could be achieved by in situ oxidation/destruction. However, this process is not applied widely in industries as the stability issue for Fenton’s reagent is the main drawback. The aim of this mini review is to summarize the developments of Electrokinetic-Fenton process on enhancing the stability of Fenton’s reagent and process efficiency in past decades. Generally, the enhancements are conducted via four paths: (1) chemical stabilization to delay H2O2 decomposition, (2) increase of oxidant availability by monitoring injection method for Fenton’s reagent, (3) electrodes operation and iron catalysts and (4) operating conditions such as voltage gradient, electrolytes and H2O2 concentration. In addition, the types of soils and contaminants are also showing significant effect as the soil with low acid buffering capacity, adequate iron concentration, low organic matter content and low aromatic ring organic contaminants generally gives better efficiency.

Woodland decline in upland Scotland

The recent article by Fenton (Fenton JH. 2008. A postulated natural origin for the open landscape of upland Scotland. Plant Ecology & Diversity 1:115–127) has argued that the landscapes of upland Scotland are treeless because of long-term deterioration of soil conditions. There are reasons for thinking that this might be the case in the absence of human activity. However, there have been considerable anthropogenic pressures on these landscapes for several millenia, documented archaeologically and palaeoecologically. Attempting to exclude these pressures from the discussion can only lead to an incomplete and misleading account of a complex series of changes involving an interaction which includes natural vegetational and environmental processes, climatic changes and human pressures.

Oncogenic Kras Promotes Chemotherapy-Induced Growth Factor Shedding via ADAM17.

Oncogenic mutations in Kras occur in 40% to 45% of patients with advanced colorectal cancer (CRC). We have previously shown that chemotherapy acutely activates ADAM17, resulting in growth factor shedding, growth factor receptor activation, and drug resistance in CRC tumors. In this study, we examined the role of mutant Kras in regulating growth factor shedding and ADAM17 activity, using isogenic Kras mutant (MT) and wild-type (WT) HCT116 CRC cells. Significantly higher levels of TGF-a and VEGF were shed from KrasMT HCT116 cells, both basally and following chemotherapy treatment, and this correlated with increased pErk (phosphorylated extracellular signal regulated kinase)1/2 levels and ADAM17 activity. Inhibition of Kras, MEK (MAP/ERK kinase)1/2, or Erk1/2 inhibition abrogated chemotherapy-induced ADAM17 activity and TGF-a shedding. Moreover, we found that these effects were not drug or cell line specific. In addition, MEK1/2 inhibition in KrasMT xenografts resulted in significant decreases in ADAM17 activity and growth factor shedding in vivo, which correlated with dramatically attenuated tumor growth. Furthermore, we found that MEK1/2 inhibition significantly induced apoptosis both alone and when combined with chemotherapy in KrasMT cells. Importantly, we found that sensitivity to MEK1/2 inhibition was ADAM17 dependent in vitro and in vivo. Collectively, our findings indicate that oncogenic Kras regulates ADAM17 activity and thereby growth factor ligand shedding in a MEK1/2/Erk1/2-dependent manner and that KrasMT CRC tumors are vulnerable to MEK1/2 inhibitors, at least in part, due to their dependency on ADAM17 activity.