A data-driven modeling approach for the sustainable remediation of persistent arsenic (As) groundwater contamination in a fractured rock aquifer through a groundwater recirculation well (IEG-GCW®)

Persistent arsenic (As) pollution sources from anthropogenic activities pose a serious threat to groundwater quality. This work aims to illustrate the application of an innovative remediation technology to remove As from a heavily contaminated fractured aquifer at a historically polluted industrial site. Groundwater circulation well (GCW) technology was tested to significantly increase and accelerate the mobilization and removal of As in the source area. The GCW extracts and re-injects groundwater at different depths of a vertical circulation well. By pumping out and reinjecting in different screen sections of the well, the resulting vertical hydraulic gradients create recirculation cells and affect and mobilize trapped contaminants that cannot be influenced by traditional pumping systems. The first 45-meter deep IEG-GCW® system was installed in 2020, equipped with 4 screen sections at different depths and with an above-ground As removal system by oxidation and filtration on Macrolite (Enki). A geomodeling approach supports both remediation and multi-source data interpretation. The first months of operation demonstrate the hydraulic effectiveness of the IEG-GCW® system in the fractured rock aquifer and the ability to significantly enhance As removal compared to conventional pumping wells currently feeding a centralized treatment system. The recirculation flow rate amounts to about 2 m3/h. Water pumped and treated by the GCW system is reintroduced with As concentrations reduced by an average of 20% to 60%. During the pilot test, the recirculating system removed 23 kg As whilst the entire central pump-and-treat (P&T) system removed 129 kg, although it treated 100 times more water volume. The P&T plant removed 259 mg As per m3 of pumped and treated groundwater while the GCW removed 4814 mg As per m3 of the treated groundwater. The results offer the opportunity for a more environmentally sustainable remediation approach by actively attacking the contamination source rather than containing the plume

Extrahepatic sources of factor VIII potentially contribute to the coagulation cascade correcting the bleeding phenotype of mice with hemophilia A

A large fraction of factor VIII in blood originates from liver sinusoidal endothelial cells although extrahepatic sources also contribute to plasma factor VIII levels. Identification of cell-types other than endothelial cells with the capacity to synthesize and release factor VIII will be helpful for therapeutic approaches in hemophilia A. Recent cell therapy and bone marrow transplantation studies indicated that K\ufcpffer cells, monocytes and mesenchymal stromal cells could synthesize factor VIII in sufficient amount to ameliorate the bleeding phenotype in hemophilic mice. To further establish the role of blood cells in expressing factor VIII, we studied various types of mouse and human hematopoietic cells. We identified factor VIII in cells isolated from peripheral and cord blood, as well as bone marrow. Co-staining for cell type-specific markers verified that factor VIII was expressed in monocytes, macrophages and megakaryocytes. We additionally verified that factor VIII was expressed in liver sinusoidal endothelial cells and endothelial cells elsewhere, e.g., in the spleen, lungs and kidneys. Factor VIII was well expressed in sinusoidal endothelial cells and K\ufcpffer cells isolated from human liver, whereas by comparison isolated human hepatocytes expressed factor VIII at very low levels. After transplantation of CD34(+) human cord blood cells into NOD/SCID\u3b3Null-hemophilia A mice, fluorescence activated cell sorting of peripheral blood showed >40% donor cells engrafted in the majority of mice. In these animals, plasma factor VIII activity 12 weeks after cell transplantation was up to 5% and nine of 12 mice survived after a tail clip-assay. In conclusion, hematopoietic cells, in addition to endothelial cells, express and secrete factor VIII: this information should offer further opportunities for understanding mechanisms of factor VIII synthesis and replenishment