Data Preservation: Final Step in the Life Cycle of a Mission

Many NASA Earth Observing System (EOS) have either already reached the end of their active life or are nearing it. Preservmissionsation of data products is a fairly well defined task for the NASA EOS Data Centers or DAACs.The Goddard Earth Sciences Data and Information Services Center (GES-DISC) has implemented a repository system, which is capable of long-term archive of documentation artifacts and other associated digital content. The existing GES-DISC Repository System is based on Fedora Commons, an open-source repository management software, for cost savings and flexibility.The first mission to utilize the GES-DISC Repository System was the High Resolution Dynamics Limb Sounder (HIRDLS) on the Aura spacecraft. Since then, the GES DISC has gathered documentation from the UARS and TOMS into the Repository. The Microwave Limb Sounder (MLS) team has begun delivering some early pre-launch documents to the GES-DISC Repository System as well. Other missions in planning or progress include AIRS, OMI, SORCE, SNPP Sounder, and TRMM

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

Requirement of mitogen-activated protein kinase kinase 3 (MKK3) for tumor necrosis factor-induced cytokine expression

The p38 mitogen-activated protein kinase is activated by treatment of cells with cytokines and by exposure to environmental stress. The effects of these stimuli on p38 MAP kinase are mediated by the MAP kinase kinases (MKKs) MKK3, MKK4, and MKK6. We have examined the function of the p38 MAP kinase signaling pathway by investigating the effect of targeted disruption of the Mkk3 gene. Here we report that Mkk3 gene disruption caused a selective defect in the response of fibroblasts to the proinflammatory cytokine tumor necrosis factor, including reduced p38 MAP kinase activation and cytokine expression. These data demonstrate that the MKK3 protein kinase is a critical component of a tumor necrosis factor-stimulated signaling pathway that causes increased expression of inflammatory cytokines

Defective T cell differentiation in the absence of Jnk1

The c-Jun NH2-terminal kinase (JNK) signaling pathway has been implicated in the immune response that is mediated by the activation and differentiation of CD4 helper T (TH) cells into TH1 and TH2 effector cells. JNK activity observed in wild-type activated TH cells was severely reduced in TH cells from Jnk1-/- mice. The Jnk1-/- T cells hyperproliferated, exhibited decreased activation-induced cell death, and preferentially differentiated to TH2 cells. The enhanced production of TH2 cytokines by Jnk1-/- cells was associated with increased nuclear accumulation of the transcription factor NFATc. Thus, the JNK1 signaling pathway plays a key role in T cell receptor-initiated TH cell proliferation, apoptosis, and differentiation

Differential involvement of p38 mitogen-activated protein kinase kinases MKK3 and MKK6 in T-cell apoptosis

The p38 mitogen-activated protein kinase (p38MAPK) is activated in response to various stimuli, including cellular stress, inflammatory cytokines and cell surface receptors. The activation of p38MAPK is predominantly mediated by the two upstream MAPK kinases MKK3 and MKK6. To study the role of the p38MAPK pathway in vivo, we generated Mkk6(–/–) mice. We examined whether T-cell apoptosis is affected in these mice and in our previously reported Mkk3(–/–) mice. Strikingly, in vivo deletion of double positive thymocytes in Mkk6(–/–) mice was impaired, whereas Mkk3(–/–) mice showed no apparent abnormality. Conversely, CD4(+)T cells from Mkk3(–/–) but not from Mkk6(–/–) mice were resistant to activation-induced cell death and cytokine-withdrawal-induced apoptosis. In peripheral CD4(+)T cells, MKK3 is induced upon stimulation, whereas MKK6 is downregulated. These results suggest a novel mechanism regulating T-cell apoptosis differentially through the p38MAPK pathway by MKK3 and MKK6