Liquid membrane system for the removal and concentration of transuranic elements

The goal of this program is to develop an efficient, reliable, and radiation-resistant modified liquid membrane system (MLMS) for the selective removal and concentration of transuranic elements (TRUs) and strontium-90 from dissolved Hanford sludge wastes. The efforts are divided into three categories: (1) demonstration and optimization of the MLMS for the TRUEX and SREX processes using simulant waste solution; (2) development of a radiation-resistant microporous divider and membrane module for testing with actual waste solutions; and (3) demonstration of the MLMS for the TRUEX and SREX processes using actual Hanford waste. Successful completion of these development efforts will yield a compact, versatile, and reliable MLMS for implementation with the TRUEX and SREX processes. The MLMS is simple, stable, more efficient, and easier to control and operate than conventional solvent-extraction processes, such as those employing centrifugal contactors. In addition, the MLMS process offers operational cost savings over the conventional technology, by exhibiting at least a 10% reduction in the consumption of extractant chemicals

Defective IL-12 production in mitogen-activated protein (MAP) kinase kinase 3 (Mkk3)-deficient mice.

The p38 mitogen-activated protein kinase (MAPK) pathway, like the c-Jun N-terminal kinase (JNK) MAPK pathway, is activated in response to cellular stress and inflammation and is involved in many fundamental biological processes. To study the role of the p38 MAPK pathway in vivo, we have used homologous recombination in mice to inactivate the Mkk3 gene, one of the two specific MAPK kinases (MAPKKs) that activate p38 MAPK. Mkk3(-/-) mice were viable and fertile; however, they were defective in interleukin-12 (IL-12) production by macrophages and dendritic cells. Interferon-gamma production following immunization with protein antigens and in vitro differentiation of naive T cells is greatly reduced, suggesting an impaired type I cytokine immune response. The effect of the p38 MAPK pathway on IL-12 expression is at least partly transcriptional, since inhibition of this pathway blocks IL-12 p40 promoter activity in macrophage cell lines and IL-12 p40 mRNA is reduced in MKK3-deficient mice. We conclude that the p38 MAP kinase, activated through MKK3, is required for the production of inflammatory cytokines by both antigen-presenting cells and CD4(+) T cells