Advanced application of nano-technological and biological processes as well as mitigation options for arsenic removal.

Arsenic (As) removal is a huge challenge, since several million people are potentially exposed (>10 µg/L World Health Organization guideline limit) through As contaminated drinking water worldwide. Review attempts to address the present situation of As removal, considering key topics on nano-technological and biological process and current progress and future perspectives of possible mitigation options have been evaluated. Different physical, chemical and biological methods are available to remove As from contaminated water/soil/wastes, where removal efficiency mainly depends on absorbent type, initial adsorbate concentration, speciation and interfering species. Oxidation is an important pretreatment step in As removal, which is generally achieved by several media such as O2/O3, HClO, KMnO4 and H2O2. The Fe-based-nanomaterials (α/ß/γ-FeOOH, Fe2O3/Fe3O4-γ-Fe2O3), Fe-based-composite-compounds, activated-Al2O3, HFO, Fe-Al2O3, Fe2O3-impregnated-graphene-aerogel, iron-doped-TiO2, aerogel-based- CeTiO2, and iron-oxide-coated-manganese are effective to remove As from contaminated water. Biological processes (phytoremediation/microbiological) are effective and ecofriendly for As removal from water and/or soil environment. Microorganisms remove As from water, sediments and soil by metabolism, detoxification, oxidation-reduction, bio-adsorption, bio-precipitation, and volatilization processes. Ecofriendly As mitigation options can be achieved by utilizing an alternative As-safe-aquifer, surface-water or rainwater-harvesting. Application of hybrid (biological with chemical and physical process) and Best-Available-Technologies (BAT) can be the most effective As removal strategy to remediate As contaminated environments.

SMAD3/Stat3 Signaling Mediates ß-Cell Epithelial-Mesenchymal Transition in Chronic Pancreatitis-Related Diabetes.

Many patients with chronic pancreatitis develop diabetes (chronic pancreatitis-related diabetes [CPRD]) through an undetermined mechanism. Here we used long-term partial pancreatic duct ligation (PDL) as a model to study CPRD. We found that long-term PDL induced significant ß-cell dedifferentiation, followed by a time-dependent decrease in functional ß-cell mass-all specifically in the ligated tail portion of the pancreas (PDL-tail). High levels of transforming growth factor ß1 (TGFß1) were detected in the PDL-tail and were mainly produced by M2 macrophages at the early stage and by activated myofibroblasts at the later stage. Loss of ß-cell mass was then found to result from TGFß1-triggered epithelial-mesenchymal transition (EMT) by ß-cells, rather than resulting directly from ß-cell apoptosis. Mechanistically, TGFß1-treated ß-cells activated expression of the EMT regulator gene Snail in a SMAD3/Stat3-dependent manner. Moreover, forced expression of forkhead box protein O1 (FoxO1), an antagonist for activated Stat3, specifically in ß-cells ameliorated ß-cell EMT and ß-cell loss and prevented the onset of diabetes in mice undergoing PDL. Together, our data suggest that chronic pancreatitis may trigger TGFß1-mediated ß-cell EMT to lead to CPRD, which could substantially be prevented by sustained expression of FoxO1 in ß-cells.