900 research outputs found

    Long-Term Preservation of NASA Heliophysics Data and Access: Where We Were and Where We're Going

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    The importance of ensuring preservation and useful access to the unique science potential of past, present and future NASA solar and space physics (i.e. heliophysics) data has been recognized since the inception of NASA but remains challenging. In this talk, I will briefly review the history of this topic and and then discuss the present NASA model for heliophysics science data management, including key current resources for finding and using data projects like the Space Physics Data Facility. I will highlight expected future directions, building on working elements of the present program and exploiting new technology, to further improve the data environment, address existing issues and anticipate emerging challenges

    The NASA Heliophysics Active Final Archive at the Space Physics Data Facility

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    The 2009 NASA Heliophysics Science Data Management Policy re-defined and extended the responsibilities of the Space Physics Data Facility (SPDF) project. Building on SPDF's established capabilities, the new policy assigned the role of active "Final Archive" for non-solar NASA Heliophysics data to SPDF. The policy also recognized and formalized the responsibilities of SPDF as a source for critical infrastructure services such as VSPO to the overall Heliophysics Data Environment (HpDE) and as a Center of Excellence for existing SPDF science-enabling services and software including CDAWeb, SSCWeb/4D Orbit Viewer, OMNIweb and CDF. We will focus this talk to the principles, strategies and planned SPDF architecture to effectively and efficiently perform these roles, with special emphasis on how SPDF will ensure the long-term preservation and ongoing online community access to all the data entrusted to SPDF. We will layout our archival philosophy and what we are advocating in our work with NASA missions both current and future, with potential providers of NASA and NASA-relevant archival data, and to make the data and metadata held by SPDF accessible to other systems and services within the overall HpOE. We will also briefly review our current services, their metrics and our current plans and priorities for their evolution

    A Proposal to Strengthen Juvenile Miranda Rights: Requiring Parental Presence in Custodial Interrogations

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    On October 31, 1997, eleven-year-old Nathaniel Abraham was at school and enjoying Halloween with his grade school classmates. The festivities ended, however, when members of the Pontiac, Michigan police department entered the classroom and arrested Nathaniel for first degree murder. Two days before, on October 29, eighteen- year-old Ronnie Lee Greene was walking out of a convenience store in Pontiac when a .22 caliber bullet struck him in the head and killed him.\u27 Police suspected Nathaniel who, at the time of his arrest, had over twenty encounters with law enforcement. Once in custody, Nathaniel eventually confessed to shooting Greene and signed a form waiving both his right to remain silent and his right to have his attorney present during questioning.3 Prior to trial, however, Family Court Judge Eugene Arthur Moore barred the confession as inadmissible at trial, finding that Nathanial was unable to understand the Miranda rights as they were read to him. The court relied on psychological evaluations that placed twelve-year-old Nathaniel\u27s mental and emotional level at that of a six or an eight year old.\u27 On April 1, 1998, the Michigan Court of Appeals reversed, finding that the confession was in fact admissible in court.\u27 After the appellate court\u27s decision, Nathaniel\u27s trial proceeded and received heavy coverage not only in Michigan but nationally as well. During the trial, news cameras followed the 4\u279 , sixty-five pound boy in and out of Michigan courtrooms.! In the fall of 1999, a jury convicted Nathaniel Abraham of first degree murder, making him one of the youngest people convicted of murder in the history of the United States.\u27 Amid the publicity stemming from the murder trial, jurists, attorneys and commentators have begun to re-examine the juvenile criminal law system and the constitutional rights afforded juveniles in that system

    A communications model for an ISAS to NASA span link

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    The authors propose that an initial computer-to-computer communication link use the public packet switched networks (PPSN) Venus-P in Japan and TELENET in the U.S. When the traffic warrants it, this link would then be upgraded to a dedicated leased line that directly connects into the Space Physics Analysis Network (SPAN). The proposed system of hardware and software will easily support migration to such a dedicated link. It therefore provides a cost effective approach to the network problem. Once a dedicated line becomes operation it is suggested that the public networks link and continue to coexist, providing a backup capability

    Glutamate Neurotransmission in Rodent Models of Traumatic Brain Injury

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    Traumatic brain injury (TBI) is a leading cause of death and disability in people younger than 45 and is a significant public health concern. In addition to primary mechanical damage to cells and tissue, TBI involves additional molecular mechanisms of injury, termed secondary injury, that continue to evolve over hours, days, weeks, and beyond. The trajectory of recovery after TBI is highly unpredictable and in many cases results in chronic cognitive and behavioral changes. Acutely after TBI, there is an unregulated release of glutamate that cannot be buffered or cleared effectively, resulting in damaging levels of glutamate in the extracellular space. This initial loss of glutamate homeostasis may initiate additional changes in glutamate regulation. The excitatory amino acid transporters (EAATs) are expressed on both neurons and glia and are the principal mechanism for maintaining extracellular glutamate levels. Diffusion of glutamate outside the synapse due to impaired uptake may lead to increased extrasynaptic glutamate signaling, secondary injury through activation of cell death pathways, and loss of fidelity and specificity of synaptic transmission. Coordination of glutamate release and uptake is critical to regulating synaptic strength, long-term potentiation and depression, and cognitive processes. In this review, we will discuss dysregulation of extracellular glutamate and glutamate uptake in the acute stage of TBI and how failure to resolve acute disruptions in glutamate homeostatic mechanisms may play a causal role in chronic cognitive symptoms after TBI

    Principal Investigator Views of the IRB System

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    We undertook a qualitative e-mail survey of federally-funded principal investigators of their views of the US human subjects protection system, intended to identify the range of investigator attitudes. This was an exploratory study with a 14% response rate. Twenty-eight principal investigators responded; their comments were analyzed to show underlying themes, which are here presented along with supporting quotations

    Traumatic Brain Injury Induces Alterations in Cortical Glutamate Uptake without a Reduction in Glutamate Transporter-1 Protein Expression

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    We hypothesize that the primary mechanism for removal of glutamate from the extracellular space is altered after traumatic brain injury (TBI). To evaluate this hypothesis, we initiated TBI in adult male rats using a 2.0 atm lateral fluid percussion injury (LFPI) model. In the ipsilateral cortex and hippocampus, we found no differences in expression of the primary glutamate transporter in the brain (GLT-1) 24 h after TBI. In contrast, we found a decrease in glutamate uptake in the cortex, but not the hippocampus, 24 h after injury. Because glutamate uptake is potently regulated by protein kinases, we assessed global serine-threonine protein kinase activity using a kinome array platform. Twenty-five kinome array peptide substrates were differentially phoshorylated between LFPI and controls in the cortex, whereas 19 peptide substrates were differentially phosphorylated in the hippocampus (fold change ≥ ± 1.15). We identified several kinases as likely to be involved in acute TBI, including protein kinase B (Akt) and protein kinase C (PKC), which are well-characterized modulators of GLT-1. Exploratory studies using an inhibitor of Akt suggest selective activation of kinases in LFPI versus controls. Ingenuity pathway analyses of implicated kinases from our network model found apoptosis and cell death pathways as top functions in acute LFPI. Taken together, our data suggest diminished activity of glutamate transporters in the prefrontal cortex, with no changes in protein expression of the primary glutamate transporter GLT-1, and global alterations in signaling networks that include serine-threonine kinases that are known modulators of glutamate transport activity

    Multivariate association analysis of the components of metabolic syndrome from the Framingham Heart Study

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    Metabolic syndrome, by definition, is the manifestation of multiple, correlated metabolic impairments. It is known to have both strong environmental and genetic contributions. However, isolating genetic variants predisposing to such a complex trait has limitations. Using pedigree data, when available, may well lead to increased ability to detect variants associated with such complex traits. The ability to incorporate multiple correlated traits into a joint analysis may also allow increased detection of associated genes. Therefore, to demonstrate the utility of both univariate and multivariate family-based association analysis and to identify possible genetic variants associated with metabolic syndrome, we performed a scan of the Affymetrix 50 k Human Gene Panel data using 1) each of the traits comprising metabolic syndrome: triglycerides, high-density lipoprotein, systolic blood pressure, diastolic blood pressure, blood glucose, and body mass index, and 2) a composite trait including all of the above, jointly. Two single-nucleotide polymorphisms within the cholesterol ester transfer protein (CETP) gene remained significant even after correcting for multiple testing in both the univariate (p < 5 × 10-7) and multivariate (p < 5 × 10-9) association analysis. Three genes met significance for multiple traits after correction for multiple testing in the univariate analysis, while five genes remained significant in the multivariate association. We conclude that while both univariate and multivariate family-based association analysis can identify genes of interest, our multivariate approach is less affected by multiple testing correction and yields more significant results
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